bluuebunny/crossref_metadata_2025_split huggingface dataset:
Phantom limb sensation
Authors: Woodhouse Annie 
Published: February 2005

SUMMARY1. Phantom limb pain and sensations are common in amputees. The present paper defines phantom limb pain, stump pain and phantom limb sensation and then gives an overview of the incidence and characteristics of the phenomena.2. Theories of phantoms are presented, including peripheral, central and supraspinal theories, with particular attention given to Melzack's neuromatrix.3. Evidence of cortical reorganization following amputation is given and the extent to which cortical reorganization contributes to phantom limb pain is discussed.
Physiological characteristics of low‐threshold mechanoreceptors in joints, muscle and skin in human subjects
Authors: Macefield Vaughan G 
Published: February 2005

SUMMARY1. The development of microneurography, in which an insulated tungsten microelectrode is inserted into an accessible peripheral or cranial nerve in awake human subjects, has allowed detailed analyses of the signalling capacities of single mechanoreceptive afferents from the skin, muscles and joints. For example, we know much about how the two classes of rapidly adapting (Meissner and Pacinian) and two classes of slowly adapting (Merkel and Ruffini) cutaneous mechanoreceptors encode forces applied normal or tangential to the skin of the hand and the similarities and differences in glabrous versus non‐glabrous skin (and receptors associated with hairs). We also know about stretch‐ and force‐sensitive endings in muscle (the muscle spindle and Golgi tendon organ, respectively) and how they behave during passive or active movements or during isometric contractions. In addition, we have characterized the firing properties of mechanoreceptors in the joint capsules of the fingers. However, we know little about sensory nerves in the periosteum, other than that nociceptors and Pacinian corpuscles exist.2. In addition to studies on the physiology of sensory endings in human subjects, microstimulation through the recording microelectrode has revealed how the brain deals with the sensory information conveyed by a single afferent. From this work, we know that there is specificity in the sensory channels: electrical stimulation of a single Meissner or Pacinian corpuscle generates frequency dependent illusions of ‘flutter’ or ‘vibration’, whereas microstimulation of a single Merkel afferent can produce a percept of ‘pressure’ and stimulation of a single joint afferent can evoke a sensation of ‘joint rotation’. Interestingly, the input from a single Ruffini ending in the skin cannot be perceived and the same is true of muscle spindle afferents. So, where does this leave us with osseoperception from the mouth? Given that the periodontal receptors in the vicinity have been lost, which mechanoreceptive endings could encode forces applied to a bone‐implanted prosthesis?3. Meissner and Merkel endings have very small receptive fields and respond only to local forces. Pacinian corpuscles have an exquisite sensitivity to brisk mechanical events and could respond to such stimuli transmitted through the bone to a remote receptor, but would not be able to encode sustained forces. Ruffini endings also respond to forces applied remote to the receptive field and, unlike the Pacinian corpuscles, respond in a sustained fashion, but would their signals be perceived? Like muscle spindles, it is possible that the coactivation of many Ruffini endings could provide meaningful information. Finally, as we have seen, the input from a single joint receptor can be perceived, but they mostly respond at the limits of joint rotation, so it is unlikely that any associated with the temporomandibular joint could contribute to osseoperception.
Neurotoxic effects of venoms from seven species of australasian black snakes (Pseudechis): Efficacy of black and tiger snake antivenoms
Authors: Ramasamy Sharmaine , Fry Bryan G , Hodgson Wayne C 
Published: February 2005

SUMMARY1. Pseudechis species (black snakes) are among the most widespread venomous snakes in Australia. Despite this, very little is known about the potency of their venoms or the efficacy of the antivenoms used to treat systemic envenomation by these snakes. The present study investigated the in vitro neurotoxicity of venoms from seven Australasian Pseudechis species and determined the efficacy of black and tiger snake antivenoms against this activity.2. All venoms (10 µg/mL) significantly inhibited indirect twitches of the chick biventer cervicis nerve–muscle preparation and responses to exogenous acetylcholine (ACh; 1 mmol/L), but not to KCl (40 mmol/L), indicating activity at post‐synaptic nicotinic receptors on the skeletal muscle.3. Prior administration of either black or tiger snake antivenom (5 U/mL) prevented the inhibitory effects of all Pseudechis venoms.4. Black snake antivenom (5 U/mL) added at t90 (i.e. the time‐point at which the original twitch height was reduced by 90%) significantly reversed the effects of P. butleri (28 ± 5%), P. guttatus (25 ± 8%) and P. porphyriacus (28 ± 10%) venoms. Tiger snake antivenom (5 U/mL) added at the t90 time‐point significantly reversed the neurotoxic effects of P. guttatus (51 ± 4%), P. papuanus (47 ± 5%) and P. porphyriacus (20 ± 7%) venoms.5. We show, for the first time, the presence of neurotoxins in the venom of these related snake species and that this activity is differentially affected by either black snake or tiger snake antivenoms.
REPERFUSION INJURY IN THE HUMAN FOREARM IS MILD AND NOT ATTENUATED BY SHORT‐TERM ISCHAEMIC PRECONDITIONING
Authors: Kilian JG , Nakhla S , Griffith K , Harmer J , Skilton M , Celermajer DS 
Published: February 2005

SUMMARY1. Ischaemia–reperfusion (IR) injury is an important contributor to tissue damage and has been shown to be attenuated by preconditioning (PC) in some animal models. A recent report has suggested that the forearm can be used for the study of this phenomenon in humans. We aimed to reproduce and further characterize this model.2. Healthy young adult volunteers (mean (±SEM) age 32 ± 6 years) were studied on two occasions. During one visit, IR alone was induced by 10 min of upper arm cuff occlusion, whereas on another occasion a PC stimulus (three 3 min cuff inflations) preceded IR. Endothelial function in the ischaemic arm was assessed by measuring arterial flow‐mediated dilatation (FMD) and by calculation of forearm blood flow at baseline and 15 and 60 min after IR. Systemic venous blood was sampled from the non‐ischaemic arm at baseline, after PC and at 2, 15 and 30 min after IR to assess neutrophil/leucocyte (CD11b) and platelet (bound glycoprotein IIb/IIIa and fibrinogen) activation, as well as numbers of platelet–leucocyte complexes, which were determined by flow cytometry. Because of a lack of measurable effects, the IR experiment was repeated with 20 min ischaemia in six subjects.3. Five females and eight males completed the study. Flow‐mediated dilatation was significantly impaired 30 min after IR (4.1 vs 6.2% at baseline; P < 0.05);however, this was not significantly attenuated by ischaemic PC (FMD reduction at 30 min compared with baseline was 2.1 ± 0.5% with IR alone and 2.6 ± 1.4% with IR after PC; NS). No significant effect was seen on the number of platelet–leucocyte aggregates or on white cell or platelet activation after IR alone or after IR with PC (P > 0.6 for all comparisons). Similar results were obtained in six subjects studied subjected to 20 min ischaemia.4. In conclusion, in healthy young adults, brief periods of skeletal muscle ischaemia lead to arterial endothelial dysfunction, but no significant platelet or white cell activation. Preconditioning does not attenuate this effect on the endothelium. Further experiments with longer ischaemia times and varying PC stimuli may be necessary to produce measurable effects; however, this may prove difficult in conscious human subjects.
Lamivudine monotherapy for spontaneous severe acute exacerbation of chronic hepatitis B
Authors: TSUBOTA AKIHITO , ARASE YASUJI , SUZUKI YOSHIYUKI , SUZUKI FUMITAKA , SEZAKI HITOMI , HOSAKA TETSUYA , AKUTA NORIO , SOMEYA TAKASHI , KOBAYASHI MASAHIRO , SAITOH SATOSHI , IKEDA KENJI , KUMADA HIROMITSU 
Published: February 2005

AbstractBackground: Severe acute exacerbations of chronic hepatitis B virus (HBV) infection can spontaneously occur and rapidly progress to fatal hepatic failure. The purpose of the present paper was to identify factors that could influence the rapid progression of liver disease to hepatic failure, and assess the effects of lamivudine on serious disease.Methods: Twenty‐five patients with spontaneous severe acute exacerbation (accompanied by jaundice and coagulopathy) were consecutively treated with lamivudine. Their clinical outcomes were compared with those of 25 lamivudine‐untreated patients, as historical controls.Results: Six lamivudine‐treated patients (24%)and seven controls (28%) rapidly developed hepatic failure. Lamivudine monotherapy did not significantly prevent progression to hepatic failure. Multivariate analysis identified baseline serum bilirubin ≥6 mg/dL (odds ratio [OR]: 5.61; 95% confidence interval [CI]: 1.66–21.61; P = 0.018), pre‐existing cirrhosis (OR: 4.52; 95%CI: 1.26–30.42; P = 0.034), and baseline prothrombin time <40% (OR: 3.75; 95%CI: 1.03–43.86; P = 0.045) as independent determinants of the event. Of the aforementioned patients with hepatic failure, three lamivudine‐treated patients (50%) and two controls (29%) survived (P > 0.15). However, lamivudine induced a sustained normalization of liver function and inhibited the development of cirrhosis in survivors.Conclusions: Lamivudine monotherapy conferred no significant protection against rapid progression of the disease to hepatic failure, but it resulted in long‐term benefits. Lamivudine combined with other drugs could be more beneficial for patients with the aforementioned risk factors.© 2004 Blackwell Publishing Asia Pty Ltd
Dual treatment of albendazole in hepatic hydatidosis: New therapeutic modality in 52 cases
Authors: POLAT CAFER , DERVISOGLU ADEM , HOKELEK MURAT , YETIM IBRAHIM , BUYUKKARABACAK YALCIN , OZKUTUK YASIN , ERZURUMLU KENAN 
Published: February 2005

AbstractBackground:  Hepatic hydatidosis still remains as a serious problem in general surgery. Recurrence and/or secondary hydatidosis rates are up to 25% in the cases treated with surgery alone. Albendazole is the most commonly used drug in the medical treatment of echinococcosis. The aim of the present study was to evaluate the effect of albendazole using the intraoperative and perioperative periods as dual therapy.Methods:  Fifty‐two cases of hepatic hydatidosis were evaluated and treated by dual treatment of albendazole together with surgery. Perioperative albendazole treatment was given in a dose of 12–15 mg/kg per day in four divided doses. The treatment started 2–28 days before the surgery when the diagnosis was established and continued for 2–24 months (4.76 ± 3.25) postoperatively in a cyclic monthly form. A total of 1.7 µg/mL albendazole solution was used as a protoscolicidal agent in the cystic cavity intraoperatively. In the postoperative period serology, ultrasonography and computed tomography evaluations were done. The follow‐up period was 5–92 months (mean: 62.48 months).Results:  There was no recurrence in the present study. One patient died in the 6th postoperative week due to cerebral hydatidosis and multiple organ failure. Early and late morbidity rates were 7.69 and 9.61%, respectively.Conclusions:  Dual albendazole treatment is effective in the prevention of recurrences and/or secondary hydatidosis.
Evidence against a role for endotoxin in the hepatic encephalopathy of rats with thioacetamide‐induced fulminant hepatic failure
Authors: CHEN CHIEN‐TING , CHU CHI‐JEN , WANG TEH‐FANG , LU REI‐HWA , LEE FA‐YAUH , CHANG FULL‐YOUNG , LIN HAN‐CHIEH , CHAN CHE‐CHANG , WANG SUN‐SANG , HUANG HUI‐CHUN , LEE SHOU‐DONG 
Published: February 2005

AbstractBackground and Aims: Endotoxin has been proposed to participate in the development of hepatic encephalopathy. However, there is no published data concerning the effects of endotoxin neutralization on the degree of hepatic encephalopathy. The present study investigated the effect of chronic intraperitoneal injection of polymyxin B, a neutralizing antagonist of endotoxin, on hepatic encephalopathy in rats with thioacetamide (TAA)‐induced fulminant hepatic failure.Methods: Male Sprague‐Dawley rats weighing 300–350 g were used. Fulminant hepatic failure was induced by intraperitoneal injection of TAA (350 mg/kg/day) for 3 days. Two series of rats were designed to compare the effects of low dose (0.1 mg) or high dose (0.2 mg) intraperitoneal polymyxin B administration versus normal saline (NS) on hepatic encephalopathy. The injection was twice daily started from 2 days prior to TAA administration and lasted for 5 days. Severity of encephalopathy was assessed by the counts of motor activity in an Opto‐Varimex animal activity meter. Plasma levels of endotoxin and tumor necrosis factor‐α (an index of liver injury) were measured by Limulus assay and the ELISA method, respectively.Results: Neutralization of endotoxin by either low dose or high dose polymyxin B administration did not significantly alleviate the degree of hepatic encephalopathy, as represented by the counts of motor activities (P > 0.05). Plasma levels of endotoxin and tumor necrosis factor‐α were comparable between rats treated with polymyxin B or NS (P > 0.05).Conclusion: Our findings do not support the notion that endotoxin plays a major role in the pathogenesis of hepatic encephalopathy in rats with TAA‐induced fulminant hepatic failure.
Altered phenotype of dextran sulfate sodium colitis in interferon regulatory factor‐1 knock‐out mice
Authors: MANNICK ELIZABETH E , COTE RAE L , SCHURR JILL R , KROWICKA HALINA S , SLOOP GREGORY D , ZAPATA‐VELANDIA ADRIANA , CORREA HERNAN , RUIZ BERNARDO , HORSWELL RONALD , LENTZ JENNIFER J , BYRNE PATRICK , GASTANADUY M MARIELLA , HORNICK CONRAD A , LIU ZHIYUN 
Published: February 2005

AbstractBackground and Aims: Interferon regulatory factor‐1 (IRF‐1) is a transcription factor with antiviral, proinflammatory and tumor suppressor properties. We examined the role of IRF‐1 in dextran sulfate sodium colitis, a murine model of inflammatory bowel disease, to determine if absence of the gene would protect against colitis.Methods: C57BL/6J mice with a targeted disruption of IRF‐1 and wild‐type C57BL/6J controls received five 7‐day cycles of 2% dextran sulfate sodium alternating with five 7‐day cycles of water. Colonic tissue was formalin fixed for histological analysis and total RNA extracted for gene chip and SYBR green real‐time polymerase chain reaction (PCR) analysis.Results: Histological analysis revealed increased distortion of crypt architecture in the dextran sulfate sodium‐treated, IRF‐1 –/– animals as compared to dextran sulfate sodium‐treated wild‐type animals. Five of 15 dextran sulfate sodium‐treated IRF‐1 –/– mice, but only one of 14 dextran sulfate sodium‐treated wild‐type mice, developed colonic dysplasia. Microarray analysis comparing colonic gene expression in IRF‐1 –/– and wild‐type animals revealed decreased expression of caspases, genes involved in antigen presentation, and tumor suppressor genes in the IRF‐1 –/– animals. Increased expression of genes involved in carcinogenesis and immunoglobulin and complement genes was also noted in the knock‐out animals.Conclusions: Absence of IRF‐1 is not protective in dextran sulfate sodium colitis.
Post‐infectious irritable bowel syndrome in patients with Shigella infection
Authors: JI SANGWON , PARK HYOJIN , LEE DOKYONG , SONG YOUNG KOO , CHOI JAE PHIL , LEE SANG‐IN 
Published: February 2005

AbstractBackground and Aims: Bacterial gastroenteritis has been known as a risk factor of irritable bowel syndrome (IBS). Several risk factors of post‐infectious IBS (PI‐IBS) have been documented. The aims of this study were to verify the role of bacterial gastroenteritis in the development of IBS and the risk factors for the development of PI‐IBS. The clinical course of PI‐IBS was also investigated.Methods: We recruited 143 patients with shigellosis during its outbreak and 113 controls. Both groups were followed up for 12 months. Bowel symptoms were evaluated by use of questionnaires at 3, 6 and 12 months after the initial recruitment.Results: Complete data were obtained from 101 patients (70.6%) and 102 healthy controls (90.3%). At 12 months, 15 patients and six controls had IBS (adjusted OR; 2.9, 95% CI; 1.1–7.9). Of the 15 patients, five had IBS symptoms consistently for 12 months, three did not have IBS symptoms initially and seven had fluctuating bowel symptoms. The duration of diarrhea was an independent risk factor of PI‐IBS.Conclusions: Bacterial gastroenteritis is a risk factor of IBS and the duration of diarrhea as the index of severity of initial illness is an independent risk factor of PI‐IBS. The clinical course of PI‐IBS is variable over the 1 year of follow‐up.
Fate of bradykinin on the rat liver when administered by the venous or arterial route
Authors: GIOLI‐PEREIRA LUCIANA , NASCIMENTO ÉCIO ALVES , SANTOS EDSON LUCAS , BRACHT ADELAR , JULIANO MARIA APARECIDA , PESQUERO JOÃO BOSCO , BORGES DURVAL ROSA , KOUYOUMDJIAN MARIA 
Published: February 2005

AbstractBackground and Aim: Bradykinin (BK) infused into the portal vein elicits a hypertensive response via the B2 receptor (B2R) and is efficiently hydrolyzed by the liver. Our purpose was to characterize the mechanism of interaction between BK and the liver.Method: BK, HOE‐140 (a B2R antagonist), des‐R9‐BK (a B1R agonist) and enzyme inhibitors were used in monovascular or bivascular perfusions and in isolated liver cell assays.Results: Des‐R9‐BK did not elicit a portal hypertensive response (PHR); BK infused into the hepatic artery elicited a calcium‐dependent PHR and a calcium‐independent arterial hypertensive response (HAHR), with the latter being almost abolished by naproxen. BK has a predominant distribution in the extracellular space and an average hepatic extraction of 8% in the steady state. Hydrolysis products of infused BK (R1‐F5 and R1‐P7) did not elicit PHR. Angiotensin converting enzyme (ACE) is concentrated in the perivenous region and B2R in the periportal region. Microphysiometry showed that BK (and not a B1 agonist) interacts with stellate cells and the endothelial sinusoidal/Kupffer cell fraction. This effect was inhibited by the B2R antagonist.Conclusions: Events can be summarized as: the hypertensive action of BK on sinusoidal cells of the periportal region is followed by its hydrolysis by ACE which is primarily present in the perivenous region; there is no functional B1R in the normal liver; BK induces HAHR via eicosanoid release and PHR by a distinct pathway on the B2R. Our data suggest that BK may participate in the modulation of sinusoidal microvasculature tonus both in the portal and the arterial routes.
Functional promotor polymorphism in RANTES gene does not influence the clinical course of Helicobacter pylori infection
Authors: HELLMIG STEPHAN , MASCHERETTI SILVIA , FÖLSCH ULRICH , SCHREIBER STEFAN 
Published: February 2005

AbstractBackground and Aims: Helicobacter pylori was found to increase the transcription of RANTES as a potent chemoattractant cytokine in mucosal inflammation. The aim of this study was to test if a functional promotor polymorphism in the RANTES gene leading to a higher transcriptional activity influences the severity of the mucosal damage in H. pylori infected individuals.Methods: A single nucleotide polymorphism, C−471T, was genotyped by TaqMan technology in a sample of 344 consecutive patients with H. pylori infection undergoing upper gastrointestinal endoscopy and 370 blood donors. Association with the development of erosions and stomach or duodenum ulcers as well as atrophic gastritis were tested.Results: None of the genotypes were associated with the severity of mucosal damage in stomach or duodenum (P > 0.05).Conclusion: Even though H. pylori itself induces expression of RANTES, at the transcriptional level, genetic variations leading to higher transscriptional activity do not modify the degree of inflammation.
Effects of potassium‐magnesium citrate supplementation on cytosolic ATP citrate lyase and mitochondrial aconitase activity in leukocytes: A window on renal citrate metabolism
Authors: TOSUKHOWONG PIYARATANA , TUNGSANGA KRIANG , PHONGUDOM SUMET , SRIBOONLUE POTE 
Published: February 2005

AbstractBackground: An increase in urinary citrate excretion is associated with a decrease in activity of renal cortical cytosolic ATP citrate lyase (ACL) and mitochondrial aconitase (m‐aconitase). Because potassium‐magnesium citrate causes an increase in urinary citrate excretion, we decided to assess its effects on ACL and m‐aconitase in the leukocytes of renal stone patients.Methods: Twenty male renal stone patients were supplemented with potassium‐magnesium citrate twice daily (i.e. 42 mEq potassium, 21 mEq magnesium, and 63 mEq citrate per day) for a period of 1 month. Two 24‐h urine and one 15‐mL heparinized blood samples were collected from each patient before and after supplementation. Urine samples were analyzed for relevant biochemical compositions. Leukocytes were separated from blood samples by centrifugation and assayed for ACL and m‐aconitase activity.Results: Supplementation with potassium‐magnesium citrate significantly increased urinary pH (P < 0.005) and excretions of potassium (P < 0.001), magnesium (P < 0.001) and citrate (P < 0.0001). The activity of both ACL and m‐aconitase were significantly decreased (P < 0.004 and P < 0.02 respectively). The decrease in ACL activity was inversely correlated with an increase in urinary excretion of both potassium (r = −0.620, P < 0.0001) and citrate (r = −0.451, P < 0.004). A similar inverse correlation was observed between m‐aconitase activity and urinary excretion of citrate (r = −0.322, P < 0.043).Conclusion: Changes in enzyme activity, related to citrate metabolism in leukocytes, might reflect the status of renal tubular cells.
Laparoscopic adrenalectomy in patients with large adrenal tumors
Authors: NAYA YUKIO , SUZUKI HIROYOSHI , KOMIYA AKIRA , NAGATA MAKI , TOBE TOYOFUSA , UEDA TAKESHI , ICHIKAWA TOMOHIKO , IGARASHI TATSUO , YAMAGUCHI KUNIO , ITO HARUO 
Published: February 2005

AbstractObjectives: The maximum size of adrenal tumors that should be removed by laparoscopic adrenalectomy is controversial. We conducted a retrospective comparison of the results of laparoscopic adrenalectomy between patients with adrenal tumors ≥6 cm (‘large tumors’) and patients with adrenal tumors <6 cm (‘small tumors’).Methods: The participants in the study were 16 patients with large tumors and 111 patients with small tumors. The patients comprised 59 men and 68 women (mean age, 49.0 years; age range, 23–79) with varying diagnoses. Of the 16 patients with large tumors, five had Cushing's syndrome, four had pheochromocytomas, six had a non‐functional tumor and one had malignant lymphoma. Adrenal tumors were confirmed by hormonal assays, biochemical tests and computed tomography. Of the 16 large tumors, five tumors were on the right and 11 were on the left.Results: We found no significant differences in general demographic parameters between patients with large and small tumors. The mean duration of surgery was not significantly different between two groups. (large tumors, 210 min; small tumors,175 min). The mean volume of blood loss was 212 mL for large tumors and 30 mL for small tumors (P < 0.001, significant difference). There was no significant difference in time until walking, duration of hospitalization or number of using analgesics used. The time to first oral intake of group 1 (<6 cm) was significantly shorter than group 2 (≥6 cm). Tumor size (≥7.5 cm) was an independent predictor of a longer operation and greater blood loss in large tumors.Conclusions: Laparoscopic adrenalectomy for large tumors was safe and minimally invasive.