bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regulation of the Urine Concentration Mechanism by the Oropharyngeal Afferent Pathway in Man
Authors: Kuramochi Gen , Kobayashi Isao 
Published: April 2003

<i>Background:</i> It has been reported that the oropharyngeal afferent pathway behaves as a first-order factor regulating body fluid. However, the neural mechanism has not yet been clear. This study was designed to elucidate the characteristics of the neural mechanism in man. <i>Methods:</i> Healthy human subjects kept either an isotonic or hypertonic solution in the oral cavity so as to moisten the oropharyngeal mucosa without intake for 20 min. Plasma vasopressin (AVP) concentration, urine volume and urine and plasma osmolalities were measured before and after the application. <i>Results:</i> The oropharyngeal application of isotonic saline induced no significant changes in plasma AVP concentration, urine volume and osmolality, while that of hypertonic saline induced a significant decrease and increase in urine volume and osmolality, respectively. The plasma AVP concentration increased significantly after the application of hypertonic saline. Mannitol also induced a significant decrease and increase in urine volume and osmolality, respectively. However, the urinary responses after the application of mannitol were delayed compared with those of hypertonic saline. There were no significant changes in plasma osmolality before and after each application. <i>Conclusion:</i> These results suggest that the oropharyngeal afferent pathway from the oropharynx to hypothalamic AVP-producing cells takes part in the thirst mechanism regulating body fluid in humans. The oropharyngeal afferent signals may behave as sodium-chloride-sensitive osmoreceptor.
One-Year Immunological Evaluation of Chronic Hemodialysis in End-Stage Renal Disease Patients
Authors: Meier P. , von Fliedner V. , Markert M. , van Melle G. , Deppisch R. , Wauters J.-P. 
Published: April 2003

<i>Background:</i> Much research has been devoted to the determination of acute leukocyte activation as well as acute cytokines production during and after blood hemodialysis membrane interaction. In contrast, few studies deal with chronic immunological evaluation of T-cell activation markers in hemodialysis. <i>Methods:</i> We evaluated different immune parameters using a modified cellulose low-flux hemophan vs. synthetic high-flux polyamide membrane during 1 year in 35 stable chronic hemodialysis patients. Leukocyte counts, lymphocyte subpopulations, T-cell activation markers (CD69, CD25, HLA-DR, CD54, CD62L, CD45RO, CD11a, CD28), complement-activation products (C3a) and serum elastase were measured at 0, 3, 6 and 12 months in the two patient groups and compared to 13 healthy control subjects. <i>Results:</i> Over dialysis time, all patients showed a significant level elevation of CD69/CD3 (p < 0.005) and CD25/ CD3 (p < 0.005) phenotypes. In contrast, HLA-DR and CD45RO remained unchanged suggesting a truncated pattern of activation. T lymphocyte subset analysis showed in both hemodialyzed groups a significant decrease in the expression of CD54 (ICAM-1) when compared to controls (p < 0.005). C3a and elastase measurements showed a significant upward trend with dialysis time in both hemodialyzed groups. <i>Conclusion:</i> Although the immunological changes seen in chronic hemodialyzed patients must be interpreted in conjunction with their basal uremic states and the membrane permeability properties, our study suggests that 1-year immunological evaluation of hemodialysis membranes biocompatibility is associated with changes in the pattern of chronic T-cell activation, which is in part related to the use of a particular membrane type. Moreover, some key molecules (CD54) are affected in patients with end-stage renal disease undergoing hemodialysis.
lntron based radiation hybrid mapping of 15 complex I genes of the human electron transport chain
Authors: Emahazion T. , Beskow A. , Gyllensten U. , Brookes A.J. 
Published: April 2003

At least 34 complex I subunits of the electron transport chain are encoded by the nuclear genome, but only 14 of these have been mapped in the human. To rapidly map additional subunits, we have performed a combination of database mining and direct “wet” experimentation to identify intron and/or 5′ upstream genomic DNA regions for 16 complex I genes. Wet experimentation was applied to 5 genes, and involved direct PCR amplification of introns by inter-exon PCR or splinkerette based PCR walking. Database mining was applied to 11 genes, and entailed the identification of incompletely spliced mRNAs and genomic CpG island clone sequences. This data was in files that carried no documentary description of the non-exon regions. Non-exon sequences were thus derived for 15 complex I genes and used to design functional gene specific PCR assays. Radiation hybrid mapping of these PCRs located 15 complex I genes to chromosomes l, 4, 5 (2 genes), 7 (2 genes), 8, 9 (2 genes), 11, 14, 16 (2 genes), 18, and 19.
Safety and Tolerability of 619C89 after Acute Stroke
Authors: Muir Keith W. , Hamilton Steven J.C. , Lunnon Martin W. , Hobbiger Stephen , Lees Kennedy R. 
Published: April 2003

<b>Background:</b> 619C89 is a use-dependent sodium channel blocker which reduces hemispheric infarction volume by up to 60% after permanent middle cerebral artery occlusion in rats. Intravenous doses of up to 1 mg/kg have been well tolerated by healthy young and elderly volunteers. This study sought to assess safety and tolerability of 619C89 in the treatment of acute stroke. <b>Methods:</b> Patients were randomised within 12 h of onset of stroke to receive 619C89 or placebo as an intravenous loading dose, followed by maintenance doses given 8 hourly for 64 h in a double-blind, ascending-dose tolerance study. Dosing commenced at 0.5 mg/kg loading plus 0.25 mg/kg/8 h maintenance for the first group and increased in increments of 0.5 mg/kg loading +0.25 mg/kg/8 h maintenance thereafter. Safety evaluation was continued for 3 months. <b>Results:</b> 48 patients were recruited. 12 received placebo and 36 received 619C89 in doses up to 2.5 mg/kg loading plus 1.25 mg/kg/8 h. Dose escalation was stopped after the occurrence of hallucinations in 5 of 18 patients who received 2 mg/kg +1 mg/kg/8 h or more. Gastro-intestinal upset and confusion were also possibly drug related. No drug-related effects on cardiovascular function were found. <b>Conclusions:</b> 619C89 was associated with significant central nervous system side-effects at doses of 2 mg/kg +1 mg/kg/8 h or greater as discrete intravenous infusions within 12 h of stroke onset. It may also cause gastro-intestinal side-effects. Doses below this are well tolerated in patients. No adverse cardiovascular effects were seen.
Pathophysiological Assessment of Nitric Oxide (Given as Sodium Nitroprusside) in Acute Ischaemic Stroke
Authors: Butterworth R.J. , Cluckie A. , Jackson S.H.D. , Buxton-Thomas M. , Bath P.M.W. 
Published: April 2003

Acute ischaemic stroke is characterised by reductions in local cerebral blood flow (CBF) and activation of circulating platelets and leucocytes. Nitric oxide is a vasodilator and can inhibit these circulating cells. The aim of this study was to assess the effect of nitric oxide on platelet function and regional CBF in patients with acute ischaemic stroke. Sodium nitroprusside (SNP), a spontaneous nitric oxide donor, was administered at a dose which caused a 10 mm Hg fall in mean arterial blood pressure (MABP) in a pathophysiological study to 22 patients with acute ischaemic stroke and 12 matched control subjects. Platelet function (whole blood aggregation and flow cytometry) was assessed before and during SNP administration. Changes in regional CBF were measured using single photon emission computerised tomography (SPECT) scanning. SNP significantly reduced platelet aggregation in both the patient and control subject groups. Equally, the expression of platelet adhesion molecules P-selectin (CD62) and glycoprotein (GP) GP IIIa (CD61) were significantly reduced in both groups. GP Ia (CDw49b) expression was significantly attenuated in the patient but not in the control group. Four patients underwent SPECT scanning and improvements in local CBF corresponding to the penumbral area of the clinical stroke site were seen in 3 of these patients. A total of 24 regions of asymmetrical perfusion were examined, pre-SNP (median (SQR)), 0.68 (0.14) vs. peri-SNP 0.78 (0.17), 2p = 0.065. SNP, given at a dose which reduced MABP by 10 mm Hg, significantly inhibited platelet aggregation and adhesion molecule expression. Improved regional CBF was seen in some patients. SNP is a candidate therapeutic agent for patients with acute ischaemic stroke and warrants further study.
Intracerebral Haemorrhage in AIDS
Authors: Roquer Jaume , Palomeras Ernest , Knobel Hernando , Pou Adolf 
Published: April 2003

We report 8 patients with the acquired immunodeficiency syndrome (AIDS) and intracerebral haemorrhage. There were 7 men and 1 woman (mean age 37.2 years) with a mean CD4 count of 81.2/mm<sup>3</sup>. Alcohol abuse was recorded in 7 patients, intravenous drug use in 4, homosexual activity in 2, thrombocytopaenia in 1 and severe hypertension in 1. There were 5 lobar and 3 deep haemorrhages. Potential aetiologies of intracerebral haemorrhage included cerebral toxoplasmosis (n = 2), thrombocytopenia (n = 2), hypertension (n = 1) and cerebral tuberculosis (n = 1). Data of these patients were compared with those of 30 AIDS inpatients without brain haemorrhage matched by age and sex and no statistically significant differences in risk factors for AIDS except for alcohol abuse (>80 g/day) (p = 0.045) were found. Causes of brain haemorrhage in AIDS patients are heterogeneous. The relationship between both conditions may be explained by the effect of several predisposing factors to stroke in association with AIDS-related complications. Intracerebral haemorrhage is a late and serious complication of AIDS (mortality 62.5%). The frequency of intracerebral haemorrhage in AIDS (1.0%) is higher than that expected in a general population of young adults.
Leukocyte Count and Aggregation during the Evolution of Cerebral Ischemic Injury
Authors: Silvestrini Mauro , Pietroiusti Antonio , Troisi Elio , Franceschelli Laura , Piccolo Paola , Magrini Andrea , Bernardi Giorgio , Galante Alberto 
Published: April 2003

We evaluated leukocyte aggregation by means of the leukergy test and count in 26 patients with atherothrombotic stroke and in 10 patients with transient ischemic attacks. The evaluation was performed within 24 h from the onset of symptoms and then repeated on day 2, 4, 6 and 8. Data were compared with those of 10 healthy controls. Stroke patients were followed until day 30 when a clinical examination and brain computed tomography were performed to evaluate the extent and outcome of cerebral damage. Both leukocyte aggregation and count were significantly increased in stroke patients with respect to controls. While leukocyte count was not able to differentiate the severity of neurological impairment in stroke patients, leukocyte aggregation was significantly higher in major than in minor stroke patients on days 2 and 4 (p < 0.05). Moreover, while values of leukocyte count recorded at entry remained substantially stable in the following determinations in all groups, leukocyte aggregation showed a significant increase (p < 0.05) on day 4 with respect to all the other determinations in major stroke patients. These findings show that the extent and temporal profile of changes in leukocyte count and aggregation are different in patients with cerebrovascular disease and suggest an involvement of altered leukocyte rheology in the development of cerebral ischemic injury.
Clinical Predictors of Early Embolic Recurrence in Presumed Cardioembolic Stroke
Authors: Arboix Adrià , García-Eroles Luis , Oliveres Montserrat , Massons Juan B. , Targa Cecilia 
Published: April 2003

<b>Background:</b> We determined clinical predictive factors of in-hospital embolic recurrence in presumed cardioembolic stroke patients by means of multivariate analysis based on clinical and neuroimaging prognostic variables assessed within 48 h of stroke onset. <b>Methods:</b> Data of 347 consecutive patients with presumed cardioembolic stroke included in a prospective stroke registry were collected. Demographic characteristics, clinical events, and outcome in the recurrent and nonrecurrent embolization group were compared. The independent predictive value of each variable on the development of early embolic recurrence was analyzed in two multiple liner regression models – one based on eight demographic, anamnestic, and clinical variables and another based on 10 clinical, neuroimaging, and outcome variables. <b>Results:</b> In-hospital recurrent embolization was diagnosed in 25 (6.9%) patients. The latency period was 12.1 days. The overall in-hospital mortality was 70.8% in the recurrent embolization group and 24.4% in the nonrecurrent embolization group (p < 0.001). Alcohol abuse, the combination of hypertension, valvular heart disease, and atrial fibrillation, nausea and vomiting, and previous cerebral infarction were predictors of recurrent embolization in the model based on clinical variables. In addition to these four variables, cardiac events were selected in the model based on clinical, neuroimaging, and outcome variables. <b>Conclusions:</b> A small number of clinical features that can be easily obtained on the patient’s initial assessment may help clinicians to identify a subgroup of patients with cardioembolic stroke at the highest risk of developing early recurrent brain or systemic embolization.
Clinician’s Biases toward Surgery in Cerebellar Hematomas: An Analysis of Decision-Making in 94 Patients
Authors: Wijdicks Eelco F. M. , St. Louis Erik K. , Atkinson John D. , Li Hongzhe 
Published: April 2003

<i>Background and Purpose:</i> No studies have examined clinical decision-making in cerebellar hemorrhages. Clinical and CT features may influence surgery in patients with a spontaneous cerebellar hematoma. One commonly accepted adage is to remove a clot when 3 cm or larger in axial diameter on presentation CT scan. It is possible that certain preferences impact on outcome. <i>Methods:</i> We analyzed 94 patients with spontaneous cerebellar hematomas between the years of 1973–1993. Thirty-one patients underwent suboccipital craniectomy and clot removal with or without ventriculostomy. Deterioration denoted worsening of consciousness, new brainstem signs, or presentation in coma. Statistical analysis was performed utilizing a tree-based model fitted by binary recursive partitioning. Ninety-five percent confidence intervals (CI) were calculated. <i>Results:</i> The overall probability of surgical intervention was 33% (CI 23–43%). The chance of surgery in stable patients was 7% (CI 2–20%). Neurologic deterioration was seen in 54 patients (57%) and increased the prospects of a surgical procedure (52%, CI 38–66%). Surgery was performed in all deteriorating patients with small hematomas (size <3 cm), but large clots (size >3 cm) did not substantially influence surgical decision-making (45%, CI 30–60%) except in patients younger than 70 years old (57%, CI 41–82%). <i>Conclusions:</i> Clinicians at our institution usually wait for clinical deterioration to unfold prior to operating on patients with cerebellar hematomas. After deterioration occurs, they prefer small hematomas but will operate on large hematomas when patients are younger than 70, generally withholding surgery from older patients. These attitudes may impact on outcome and should be considered in future treatment trials.
Patient Understanding of Genetic Principles and Their Expectations of Genetic Services within the NHS: A Qualitative Study
Authors: Emery Jon , Kumar Satinder , Smith Helen 
Published: April 2003

<b>Objectives:</b> To explore patients’ accounts of their understanding of heredity and genetic risk, the information patients believe they require to understand inherited disease, and their expectations and attitudes towards the provision of genetic services in the NHS. <b>Method:</b> Qualitative study using semi-structured, in-depth interviews of 19 patients with a family history of colorectal cancer referred to the Wessex regional cancer genetics clinic. <b>Results and Interpretation:</b> Three important themes emerged from the data: (1) Understanding genetics. (2) Making sense of genetic risk. (3) The role of primary care in genetics. Patients’ understanding of genetics is often disparate from the scientific explanation, but they feel it is unnecessary to understand basic principles of genetics to make sense of their family history of cancer. When presented with genetic risk in numerical terms, patients reformulate this information and reconstruct their risk according to personal and family experiences of cancer and personal understanding of inheritance. Although not scientifically accurate, patients’ conceptualisation of risk provides a framework on which to plan ways to reduce their own and their family’s risk of cancer. Patients perceive general practitioners predominantly as gatekeepers to secondary care with primary care currently unprepared to deal with genetic issues. <b>Conclusions:</b> This study has generated some important hypotheses relating to patients’ attitudes towards the role of primary care in genetics, and to communicating information about genetics and risk. Further research is required to explore the acceptability of genetic advice in primary care, and the value of discussing genetic risk in relation to patients’ beliefs about inheritance.
Fetomaternal Attachment and Anchorage inthe Early Diffuse Epithel iochorial Placenta of the Camel <i>(Camelus dromedarius)</i>
Authors: Abd-Elnaeim M.M. , Pfarrer C. , Saber A.S. , Abou-Elmagd A. , Jones C.J.P. , Leiser R. 
Published: April 2003

Placentae of 22 one-humped camel concepti with crown-rump lengths (CRL) ranging from 2.5 to 26 cm were studied. The placentae were processed for light, transmission and scanning electron microscopy of exposed surfaces and microvascular corrosion casts. In very early stages of pregnancy (2.5–4.5 cm CRL) three froms of fetomaternal interrelationship are described. (1) Precontact, where the mononuclear trophoblast cells are still separated from the uterine epithelium by a gap containing interareolar histotroph. Both fetal and maternal epithelia develop apical ectoplasmic pads in this location. (2) Apposition, where microvilli of the apical cell membrane of the trophoblast contact the uterine epithelium focally. Multinuclear trophoblast giant cells develop beside the population of already present mononuclear trophoblast cells. Uterine ectoplasmic pads can be observed. (3) Adhesion occurs when apical cell membranes of fetal and maternal epithelia adhere to each other closely, thus forming a ‘normal’ intercellular space of 20 nm width, without any intervening uterine luminal space. Microvillous interdigitation in this location varies from a non-microvillous ‘smooth adhesion’, to a distinctly villiform ‘rough adhesion’, and a ‘semismooth adhesion’ is achieved when trophoblastic microvilli make intimate contact with the non-microvillous uterine apical cell membranes of ectoplasmic pads. This fetomaternal attachment process is sufficient until the conceptus reaches approximately 9 cm CRL. Then, from 10 to 13 cm CRL, additional anchorage of the placenta to the endometrium is accomplished by the growth of temporary grooves and ridges of the allantochorion and the endometrium, which indent each other in a complementary fashion. The height of these groove-ridge structures increases gradually in 14 to 18 cm CRL fetuses, and they also widen at about 25 cm CRL, thus forming globular fetal troughs and irregular, thick maternal ridges. These together create units responsible for improved fetomaternal anchorage and metabolic exchange for the increasing needs of the growing fetus.
BDNF and NGF Afford in vitro Neuroprotection against Ethanol Combined with Acute Ischemia and Chronic Hypoglycemia
Authors: Mitchell J.Jean , Paiva Michael , Walker DonW. , Heaton MarietaBarrow 
Published: April 2003

Consumption of alcohol during pregnancy can result in central nervous system deficits in infants ranging from fetal alcohol effects to fetal alcohol syndrome. Changes in cerebral metabolism causing ischemic in utero conditions can also result from ethanol (EtOH). Growth factors have been shown to ameliorate ischemic damage and EtOH-induced neurotoxicity. However, using an in vitro model system of fetal alcohol effects/fetal alcohol syndrome, this study examines the neuroprotective effects of nerve growth factor, brain-derived neurotrophic factor, or glial cell line derived neurotrophic factor against EtOH treatment (0, 200, 400, 800, or 1,600 mg/dl) combined with acute ischemia (2-hour hypoxia in EtOH-containing glucose-free media) followed by chronic hypoglycemia (16-hour glucose deprivation in EtOH-containing media). 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assays assessed relative neurotoxicity. Glial cell derived neurotrophic factor was not neuroprotective. Nerve growth factor protected against ischemia/hypoglycemia combined with 0–1,600 mg/dl EtOH. Brain-derived neurotrophic factor protected against ischemia/hypoglycemia combined with 0–800 mg/dl EtOH. These studies demonstrate marked growth factor neuroprotection against a myriad of conditions encountered by developing EtOH-exposed fetuses.
Difference in Hepatic Tissue Oxygenation between Total Vascular Exclusion and Inflow Occlusion of the Liver and the Possible Role of Hepatic Venous Blood under Liver Ischemia
Authors: Sato Tsutomu , Asanuma Yoshihiro , Kusano Tomoyuki , Sasaki Noriaki , Shindo Yoshiaki , Koyama Kenji 
Published: April 2003

The difference between total vascular exclusion (TVE) and inflow occlusion (IO) of the liver was assessed by the extent of DNA injury in rats and by hepatic tissue oxygen saturation (SahtO<sub>2</sub>) in pigs. Moreover, the role of hepatic venous blood under liver ischemia was discussed. Seventy percent of the rat livers were exposed to complete IO (hepatic artery + portal vein) or to TVE (IO + hepatic vein) for 30 or 60 min. DNA strand breaks following blood flow interception were measured using the in situ nick translation technique as an indicator of liver damage. IO/TVE were performed on pigs as well under portosystemic bypass, and the oxygen saturation of the hepatic venous blood (SahvO<sub>2</sub>) was altered by changing the fraction of inspiratory oxygen or by oxygenating the inferior caval blood using an extracorporeal membrane oxygenator. The changes in SahtO<sub>2</sub> were measured sequentially using near-infrared spectroscopy. The results were as follows: (1) DNA injury occurred more severely under TVE than under IO of the rat liver at the end of ischemia, as well as 30 min after revascularization. (2) SahtO<sub>2</sub> during TVE was significantly lower than that during IO. (3) The increase in SahvO<sub>2</sub> by oxygenation of the inferior caval blood resulted in the elevation of SahtO<sub>2</sub> under IO. In conclusion, TVE could cause greater damage to the liver than IO due to the lack of the hepatic venous blood. Hepatic venous blood might play an important role in hepatic tissue oxygenation in the case of hepatic blood flow interception.