123rc/medical_text huggingface dataset:
Vulvar intraepithelial neoplasia. A clinicopathologic study of 60 cases. Sixty cases of vulvar intraepithelial neoplasia (VIN) were analyzed clinicopathologically (24 VIN I, 9 VIN II, 27 VIN III). The ages of the patients ranged from 21 to 83 years (mean, 53.7). Colposcopic examinations showed the presence of white areas in 29 cases, red areas in 9, acetowhite areas in 6 and other alterations in 13. One-third of the lesions were multifocal. Pruritus and burning were present in 65% of the cases. Fifty-one percent of the cases showed histologic changes suggestive of human papillomavirus (HPV) infection; the mean age of those patients was significantly lower than that of patients without HPV infection. In 15 cases of VIN, HPV DNA testing was performed with Southern blot hybridization; in three (20%) of those specimens HPV 16 episomal DNA was identified. Epithelial alterations surrounding the areas of VIN were found in 24 cases (40%)-23 squamous cellular hyperplasias and 1 lichen sclerosus. Different types of treatment were performed according to the different grades of VIN: medical therapy, diathermocoagulation, local excision, hemivulvectomy and total vulvectomy. Follow-up was possible in 52 cases, with a mean of 33 months (range, 3-98). Two cases of VIN I showed progression of disease over 12-24 months.
Pharmacological characterization of LY233053: a structurally novel tetrazole-substituted competitive N-methyl-D-aspartic acid antagonist with a short duration of action. This study reports the activity of a structurally novel excitatory amino acid receptor antagonist, LY233053 [cis-(+-)-4-[(2H-tetrazol-5-yl)methyl]piperidine-2-carboxylic acid], the first tetrazole-containing competitive N-methyl-D-aspartic acid (NMDA) antagonist. LY233053 potently inhibited NMDA receptor binding to rat brain membranes as shown by the in vitro displacement of [3H] CGS19755 (IC50 = 107 +/- 7 nM). No appreciable affinity in [3H]alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) or [3H]kainate binding assays was observed (IC50 values greater than 10,000 nM). In vitro NMDA receptor antagonist activity was further demonstrated by selective inhibition of NMDA-induced depolarization in cortical wedges (IC50 = 4.2 +/- 0.4 microM vs. 40 microM NMDA). LY233053 was effective after in vivo systemic administration in a number of animal models. In neonatal rats, LY233053 selectively blocked NMDA-induced convulsions (ED50 = 14.5 mg/kg i.p.) with a relatively short duration of action (2-4 hr). In pigeons, LY233053 potently antagonized (ED50 = 1.3 mg/kg i.m.) the behavioral suppressant effects of 10 mg/kg of NMDA. However, a dose of 160 mg/kg, i.m., was required to produce phencyclidine-like catalepsy in pigeons. In mice, LY233053 protected against maximal electroshock-induced seizures at lower doses (ED50 = 19.9 mg/kg i.p.) than those that impaired horizontal screen performance (ED50 = 40.9 mg/kg i.p.). Cholinergic and GABAergic neuronal degenerations after striatal infusion of NMDA were prevented by single or multiple i.p. doses of LY233053. In summary, the antagonist activity of LY233053 after systemic administration demonstrates potential therapeutic value in conditions of neuronal cell loss due to NMDA receptor excitotoxicity. The relatively short duration of action of LY233053 may make this compound particularly advantageous as a neuroprotective agent in the treatment of acute conditions such as cerebral ischemia.
Hemodynamic effects of renin inhibition by enalkiren in chronic congestive heart failure. Previous efforts to block the renin-angiotensin system in patients with chronic congestive heart failure (CHF) have focused on 2 distal sites in the system, the angiotensin-converting enzyme and the angiotensin II receptor. Recent work, however, has led to the development of agents that directly inhibit renin, the proximal step in the cascade. In this study, we investigated the hemodynamic effects of renin inhibition in 9 patients with chronic CHF by using enalkiren, a primate-selective, dipeptide renin inhibitor, which has been previously shown to suppress plasma renin activity and to lower blood pressure in hypertensive patients. The acute intravenous administration of enalkiren (1.0 mg/kg) produced increases in cardiac index (2.0 +/- 0.3 to 2.3 +/- 0.1 liter/min/m2) and stroke volume index (26 +/- 3 to 34 +/- 4 ml/m2) and decreases in left ventricular filling pressure (31 +/- 3 to 25 +/- 3 mm Hg), mean right atrial pressure (15 +/- 1 to 13 +/- 2 mm Hg), heart rate (78 +/- 5 to 72 +/- 6 beats/min) and systemic vascular resistance (2,199 +/- 594 to 1,339 +/- 230 dynes.s.cm-5) (all p less than 0.01 to 0.05). These observations indicate that renin inhibition produces hemodynamic benefits in patients with chronic CHF and could potentially provide a novel approach to interfering with the renin-angiotensin system in patients with this disorder.
Laser angioplasty: results of a prospective, multicenter study at 3-year follow-up. A prospective multicenter trial was initiated to evaluate the efficacy and safety of laser angioplasty. Laser recanalization was performed in 338 patients with arteriosclerotic femoropopliteal artery occlusions (average length, 8.5 cm). Neodymium-yttrium-aluminum-garnet lasers were used in combination with sapphire probe catheters. The initial recanalization rate was 85%. Complications were observed in 14% of the patients. Emergency surgery was required in 1.5%. The cumulative long-term patency rate of the successfully recanalized arteries was 80%, 70%, 62%, and 57% at 6 months, 1 year, and 2 and 3 years, respectively. The patency rates were not affected by the length of the occlusion and the long-term medication (platelet inhibition vs anticoagulation), but patients with a normal runoff had significantly better patency rates than those with reduced runoff (63% vs 52%, P less than .01). The study has shown that laser-assisted angioplasty is safe and at least as effective as conventional angioplasty.
Mutational hotspot in the p53 gene in human hepatocellular carcinomas Human hepatocellular carcinomas (HCC) from patients in Qidong, an area of high incidence in China, in which both hepatitis B virus and aflatoxin B1 are risk factors, were analysed for mutations in p53, a putative tumour-suppressor gene. Eight of the 16 HCC had a point mutation at the third base position of codon 249. The G----T transversion in seven HCC DNA samples and the G----C transversion in the other HCC are consistent with mutations caused by aflatoxin B1 in mutagenesis experiments. No mutations were found in exons 5,6,8 or the remainder of exon 7. These results contrast with p53 mutations previously reported in carcinomas and sarcomas of human lung, colon, oesophagus and breast; these are primarily scattered over four of the five evolutionarily conserved domains, which include codon 249 (refs 4-9). We suggest that the mutant p53 protein may be responsible for a selective clonal expansion of hepatocytes during carcinogenesis.
Is fibrillation chaos? Ventricular fibrillation is examined to determine whether it is an instance of deterministic chaos. Surface ECGs from dogs in fibrillation were used to generate a state space representation of fibrillation. Our analysis failed to identify a low-dimensional attractor that could be associated with fibrillation. The results suggest that fibrillation is similar to a nonchaotic random signal. We note, however, that such random-looking but nonchaotic behavior can also be generated by a nonlinear deterministic system.
Incidence and clinical significance of ST segment elevation after electrical cardioversion of atrial fibrillation and atrial flutter. To study the incidence and clinical significance of postshock ST segment elevations, we recorded 12-lead ECGs immediately after transthoracic direct-current electrical cardioversion in 146 patients with atrial fibrillation or flutter. Among 23 patients (19%), acute ST segment elevations amounted to 1.4 +/- 0.8 mV (mean +/- SD) and occurred after 243 +/- 114 joules (cumulative dose) in the precordial leads only in 14, concomitantly in precordial and inferior leads in two, and in the precordial and anterolateral leads in seven. They normalized within 1.5 +/- 0.8 minutes. Occurrence of ST segment elevation was related to previous pericardiotomy (p less than 0.00001) and age (p = 0.01). Estimation of myocardial enzyme release did not show evidence of myocardial damage. Patients with ST segment elevations had a lower conversion rate (48% versus 76%, p = 0.005). Long-term maintenance of sinus rhythm was also diminished (35% versus 59%, p = 0.03). Results of this study show that postcardioversion ST segment elevation occurs predominantly in postpericardiotomy patients and may be associated with an unfavorable arrhythmia prognosis.
Superficial esophageal carcinoma. Surgical treatment and the results. We report 92 patients treated with esophagectomy for superficial esophageal carcinoma (SEC; 9.1% of all resected esophageal cancers at our institution). The operative mortality rate was 5.4%. In 24 cases, cancer invasion was limited to the mucosa, and in 68 to the submucosa. Twenty-three patients in the former group had no lymph node involvement, whereas 24 patients (35.3%) of the latter group had lymph node metastases. The 5-year survival rate after surgery for patients with SEC limited to the mucosa was 83.5%, which was significantly better than that for carcinoma invading the submucosa (54.9%). No recurrent disease occurred in patients with lesions limited to the mucosa. In conclusion, an esophagectomy with wide lymphadenectomy is necessary to provide a better prognosis for SEC invading the submucosa, whereas a less extensive treatment may be considered for SEC limited to the mucosa.
The role of the facial nerve latency test in the prognosis of Bell's palsy. Eighty patients with idiopathic facial nerve palsy were evaluated by the facial nerve latency test. Depending on the latency time, the patients were classified into the following four groups: group A patients had normal latency times (3.25 msec); group B patients had slightly extended latency times (4 to 7 msec) and a mean of 5.6 msec; group C patients had extended latency times (10 to 14 msec) and a mean of 10.2 msec; and group D patients displayed complete disappearance of evoked compound muscle action potential (no responses). Under the same therapeutic regimen, it was determined that, when the latency time was normal or close to normal, the functional recovery of the nerve was complete or almost complete, and the recovery time was short. When the latency time was extended or there was no response, the functional recovery of the nerve was either incomplete or absent.
Compensation and overcompensation in congestive heart failure. The compensatory mechanisms that develop in response to heart failure have been well defined. In this review, it is argued that each compensatory mechanism leads to overcompensation and that there is no way to distinguish between the beneficial aspects of the former and the harmful effects of the latter. Therapeutic agents that maintain rather than decrease blood pressure might perhaps be more beneficial because of the crucial role of hypotension in initiating both compensation and overcompensation.
Intranasal administration of neostigmine potentiates both intravenous and intranasal growth hormone (GH)-releasing hormone-induced GH release in short children. Administration of cholinergic agonists increases both basal and GH-releasing hormone (GHRH)-induced GH secretion, probably acting via inhibition of endogenous somatostatin release. The aim of our study was to verify in two groups of children with idiopathic short stature the effect of intranasal administration of neostigmine (inNS; 3 mg), a cholinesterase inhibitor, on basal GH levels as well as on the somatotroph response to GHRH when the peptide was administered either iv (ivGHRH; 1 microgram/kg) or intranasally (inGHRH; 10 micrograms/kg). In group A (n = 6; age, 10.6-16.0 yr) inNS induced a significant GH increase [inNS vs. saline, area under the curve (AUC; mean +/- SEM), 263.7 +/- 60.2 vs. 73.8 +/- 3.1 micrograms/L.h; P less than 0.03] and potentiated the somatotroph response to ivGHRH (inNS with ivGHRH vs. ivGHRH, 1316 +/- 183.0 vs. 644.9 +/- 154.5 micrograms/L.h; P less than 0.03). In group B (n = 6; age, 11.5-15.9 yr) ivGHRH induced a GH rise clearly higher than that induced by inGHRH (604.2 +/- 154.3 vs. 137.1 +/- 28.2 micrograms/L.h; P less than 0.03). Administration of inNS induced a GH rise similar to that occurring after inGHRH (AUC, 239.2 +/- 69.5 micrograms/L.h) and markedly increased the inGHRH-induced GH response (482.4 +/- 103.6 micrograms/L.h; P less than 0.05 and 0.03 vs. inNS and inGHRH, respectively), so that it overlapped with that induced by ivGHRH alone. In conclusion, cholinergic agonists such as neostigmine are able to increase both basal and GHRH-induced GH secretion in short children even when given intranasally. Combined intranasal administration of neostigmine and GHRH (10 micrograms/kg) is able to induce a GH rise similar to that induced by ivGHRH alone (1 microgram/kg), suggesting the potential usefulness of this combination cocktail and route of administration for the treatment of short stature.
Recurrent urethral stricture disease managed by clean intermittent self-catheterization. We studied 41 patients with urethral stricture who had failed at least 1 operation, and were being maintained with filiform and follower dilation every 6 to 12 weeks. The patients were instructed in clean intermittent self-catheterization with a 16F red rubber catheter, which was performed every 1 to 30 days. Followup from 9 to 36 months revealed excellent compliance and average peak uroflow rates increased from 5.5 cc per second before dilation to 17.1 cc per second at the last followup visit. Clean intermittent self-catheterization is a simple method to maintain a patent urethra and obviates the need for further operations or painful dilations.
Concurrence of malignant hyperthermia and congenital abnormalities. Two children about to undergo corrective surgery were required to be investigated for malignant hyperthermia (MH). These investigations arose out of concern by the anesthetist who had obtained a history of unexplained pyrexial reactions to anaesthetic in other members of the family. Because over the years we have encountered several children with multiple congenital abnormalities who have been found to be susceptible to MH, we stressed the advisability of biopsying not only the patient but also the patient's parents. Positive responses for MH were obtained in the patients and in one of the parents on each occasion. The hypothesis of intrauterine MH with its pharmacogenetic propensity for heat production is considered as a possible etiological factor which may cause abnormalities of a congenital nature.
Effects of calcium channel blockers on coronary vasoconstriction induced by endothelin-1 in closed chest pigs. The purpose of this study was to determine the effects of endothelin-1 on the coronary vascular bed of closed chest pigs. Endothelin-1 (3 to 30 pmol/kg body weight) was selectively administered into the left anterior descending coronary artery. Coronary blood flow and epicardial vessel diameter were measured by quantitative arteriography. Arterial pressure increased after a 30 pmol/kg dose and heart rate was not changed. Coronary blood flow and vessel diameter of the left anterior descending artery significantly decreased by 74% and 32%, respectively (p less than 0.01 versus control) after the 30 pmol/kg dose, whereas these variables modestly decreased in the left circumflex artery. Endothelin-1 in doses of 10 to 30 pmol/kg produced electrocardiographic ST segment elevation associated with decreased oxygen saturation of coronary sinus venous blood. Endothelin-induced coronary vasoconstriction was significantly inhibited after treatment with intravenous diltiazem (0.2 mg/kg, n = 6) or nifedipine (0.1 mg/kg, n = 5), but not after vehicle administration (n = 4). This study demonstrates that intracoronary administration of endothelin-1 causes significant myocardial ischemia through coronary vasoconstriction, which is inhibited by a calcium channel blocker. The data suggest that calcium influx into the smooth muscle cells appears to be involved at least in part in the mechanism of endothelin-induced coronary vasoconstriction in vivo.
The effect of somatostatin on 5-hydroxytryptamine release from a carcinoid tumor. One of the major manifestations of the carcinoid syndrome is secretory diarrhea thought to be due to overproduction of 5-hydroxytryptamine (5-HT). Synthetic somatostatin analogues have proved to be clinically effective in controlling this diarrhea. We have established a continuous cell line from a human pancreatic carcinoid tumor that secretes 5-HT. We examined the ability of the somatostatin analogue, SMS 201-995, to inhibit 5-HT release in vitro. Tumor cells were exposed to SMS 201-995 (10(-6) mol/L), pentagastrin (10(-9) mol/L), acetylcholine (10(-5) mol/L), and isoproterenol (10(-5) mol/L) alone and in combination; 5-HT release was assayed with high pressure liquid chromatography. We found that pentagastrin (6.43 +/- 0.64 ng/ml), isoproterenol (20.24 +/- 2.17 ng/ml), and acetylcholine (12.39 +/- 1.10 ng/ml) each stimulated release of 5-HT compared to control values (4.38 +/- 0.42 ng/ml). SMS 201-995 significantly reduced release of 5-HT in response to isoproterenol and acetylcholine but did not inhibit the effect of pentagastin. These data suggest that different agents do not act through the same pathway to stimulate 5-HT release from human pancreatic carcinoid cells.
Long-term psychosocial adjustment to coronary artery disease. Personality hardiness, which has been conceptualized as a potential internal resource facilitating stress resistance, was examined in conjunction with Type A behavior, perceived family cohesion and adaptability, and sociodemographic and medical variables to assess the independent differential correlations of these factors with long-term psychosocial adjustment to coronary artery disease. One hundred twenty-eight patients completed the third generation Hardiness Scale, together with questionnaires measuring Type A behavior, perceived family cohesion and adaptability, and psychosocial adjustment to illness. The results showed that personality hardiness was the most salient correlate of psychosocial adjustment. High hardiness scores were associated with good adjustment to the various life domains. Angina severity accounted for the variance in social domains, but not the psychologic distress domain. Type A behavior, both dimensions of perceived family dynamics, and the sociodemographic variables did not have a significant role in explaining the variance in psychosocial adjustment. We conclude that personality hardiness could serve as a valid indicator of long-term psychosocial adjustment in patients with coronary artery disease.
Fragmented atrial activity in patients with transient atrial fibrillation. Prediction of atrial fibrillation (AF) is very important in patients with Wolff-Parkinson-White syndrome or in the selection of pacemaker therapeutic modality. In 25 patients with transient AF, the response of the atrial activity width to extrastimuli was examined in comparison with 25 patients without AF to see if the results could be used as an index of subsequent occurrence of AF. Programmed electrical stimulation using eight basic stimuli followed by single or double extrastimuli (P1P2 or P1P2P3) were delivered to the high right atrium, and the atrial activities were examined. The prolongation of the atrial activity caused by extrastimuli was termed fragmentation (Frg), and it was defined as the prolongation of more than 150% of the basic stimuli. Frg zone was defined as the zone of coupling intervals of the extrastimuli (P1P2 or P2P3) that caused Frg, and delta max Frg was defined as the difference between the widest Frg and the atrial wave width during basic stimuli. Fragmentation was reproducibly induced by extrastimuli, and there was an inverse relationship between Frg duration and the coupling interval of the extrastimuli (P1P2 or P2P3). Frg zone and delta max Frg were wider and longer in patients with transient AF in comparison with the control group for both single and double extrastimuli (p less than 0.001). AF inducibility using double extrastimuli was significantly high in patients with AF.
Right coronary artery injury during tricuspid valve annuloplasty. An unusual complication after tricuspid valve annuloplasty is described where a ring suture ligated right coronary artery and precipitated myocardial infarct and patient death. The need for caution to prevent this complication with such surgery is emphasized.
Extended release felodipine in essential hypertension. Variations in blood pressure during whole-day continuous ambulatory recording. Intraarterial blood pressure (BP) monitoring during free ambulation (Oxford technique) was carried out in 12 essential mild-to-moderate hypertensive patients undergoing 4 weeks treatment with felodipine, 10 mg given once daily in an extended release formulation. Compared to placebo, felodipine significantly reduced systolic and diastolic blood pressure throughout 24 h. The greatest reduction was observed at 10 AM, 3 h after drug administration (-32 +/- 6/-24 +/- 5 mm Hg for systolic and diastolic BP, respectively, P less than .001). Hourly BP values remained significantly lower up to and including the 24th hour during felodipine extended release treatment (-18 +/- 5/-11 +/- 3 mm Hg, P less than .001). Felodipine extended release also reduced 24 h blood pressure variability, evaluated on the standard deviation of each hourly mean (from 16.3 +/- 0.9/12.6 +/- 0.6 to 13.4 +/- 0.6/10.4 +/- 0.6 mm Hg, P less than .01). Furthermore, absolute BP values dropped significantly at the peaks of dynamic exercise (bicycle ergometer: from 248 +/- 13/123 +/- 11 to 204 +/- 24/102 +/- 13 mm Hg, P less than .001), isometric exercise (hand grip: from 232 +/- 18/133 +/- 16 to 180 +/- 20/101 +/- 16 mm Hg, P less than .001), and cold pressor test (from 229 +/- 20/127 +/- 14 to 178 +/- 22/99 +/- 15 mm Hg, P less than .001). In conclusion, felodipine extended release exerts a good antihypertensive effect which is maintained for 24 h and reduces the level of blood pressure peaks reached under different physical stresses.
Should alcoholics compete equally for liver transplantation? The circumstances of liver transplantation are unique among organ transplantation because of the dire, absolute scarcity of donor livers and the predominance of one disease--alcohol-related end-stage liver disease--as the principal cause of liver failure. We propose that patients who develop end-stage liver disease through no fault of their own should have higher priority for receiving a liver transplant than those whose end-stage liver disease results from failure to obtain treatment for alcoholism. We base our proposal on considerations of fairness and on whether public support for liver transplantation can be maintained if, as a result of a first-come, first-served approach, patients with alcohol-related end-stage liver disease receive more than half the available donor livers. We conclude that since not all can live, priorities must be established for the use of scarce health care resources.