123rc/medical_text huggingface dataset:
Teniposide (VM-26) and continuous infusion cytosine arabinoside for initial induction failure in childhood acute lymphoblastic leukemia. A Pediatric Oncology Group pilot study. Twenty-six evaluable children with newly diagnosed acute lymphoblastic leukemia (ALL) who failed to achieve initial remission after receiving two to seven drugs for at least a 4-week period were given teniposide (VM-26) and continuous infusion cytosine arabinoside (Ara-C). Twenty-two received 150 mg/m2 of VM-26 on days 1 and 2 with 100 mg/2 of Ara-C as a continuous infusion on days 1 through 5; a second shortened course was given on day 14 to eight patients who had evidence of some antileukemic effect or were clinically judged able to tolerate a second course. The last four patients received three daily doses of VM-26 and a 7-day infusion of Ara-C at the same daily dosages. Twelve (48%) achieved complete remission (CR) of ALL. There was a trend toward decreasing response rates with an increasing number of drugs used in the initial induction regimen, i.e., five CR among seven patients with a prior two-drug induction attempt, six CR among 14 patients with a prior three- to four-drug induction attempt, and one CR among four patients with a prior five- to seven-drug induction attempt (P = 0.14). Ten of 17 non-T-cell patients and two of nine T-cell patients achieved remission (P = 0.10). The median time required to achieve a complete remission from the initiation of treatment was 26 days (range, 14-72 days). This period was shorter in those who required one course compared with those who required two induction courses, i.e., 25 days median vs. 44 days median. Toxicity was significant and due mainly to marrow aplasia and infection; one patient had severe prolonged VM-26-induced hypotension. Of the 12 patients entering remission, two were removed for marrow transplant and one was removed due to parental request. In the remaining nine patients, median remission duration was only 2 months (range, 1-18 months). All nine patients relapsed in the marrow. Among the entire group of 26 patients, only one patient is alive and a long-term event-free survivor (after allogeneic marrow transplant). Due to the current use of more aggressive initial induction regimens and the extremely poor prognosis in children who fail to achieve initial remission, more intensive regimens of continuation therapy or alternative therapies, such as bone marrow transplant, should be considered.
Increase of calmodulin activator in hypertension. Modulation by dietary sodium and calcium. The aim of this study was to investigate the effects of dietary calcium and sodium on blood pressure (BP) in normotensive rats (Wistar, WKY), spontaneously hypertensive rats (SHR) and Dahl rats and on calmodulin (CaM) activator, a newly-discovered hydrophobic compound that increases CaM activity in SHR and spontaneously hypertensive mice (SHM) tissues (J Clin Invest 82:276, 1988). The CaM activator was assessed by its capacity to stimulate a CaM-dependent phosphodiesterase (CaM-PDE). In Wistar rats, which were fed a high sodium diet (3.5%), BP significantly increased (P less than .01) from 106 +/- 4 to 128 +/- 8 mm Hg in parallel to an elevation of the CaM activator from 1.57 +/- 0.14 to 2.80 +/- 0.18 U. WKY, SHR, and Dahl salt-sensitive (DS/JR) and salt-resistant (DR/JR) rats were given low (0.15%) or high (2.5%) Ca diets, both with 1% sodium. In rats receiving high dietary Ca the progression of hypertension diminished and BP was lower in SHR (156 +/- 4 mm Hg) and young DS/JR rats (125 +/- 3 mm Hg) than in those receiving low dietary Ca (192 +/- 10 and 183 +/- 2 mm Hg). There was a concomitant decrease of CaM activator in these animals to levels indistinguishable from those of WKY or DR/JR rats. The activator was also found in the heart, kidneys and erythrocytes from SHM. In the presence of exogenously added CaM, lipidic extracts from the SHM heart showed augmented CaM-PDE activity relative to normotensive preparations. This difference was eliminated by trifluoperazine.
Serum cholesterol levels and survival in elderly hypertensive patients: analysis of data from the European Working Party on High Blood Pressure in the Elderly. The relation between serum cholesterol and mortality was investigated in 822 elderly hypertensive patients randomly assigned to treatment with diuretics, with or without methyldopa, or placebo. Cox's proportional hazards model showed that pretreatment serum total cholesterol levels were independently and inversely correlated with total mortality (p = 0.03), noncardiovascular mortality (p = 0.02), and cancer mortality (p = 0.04) during treatment. Total and noncardiovascular mortality were also negatively correlated with pretreatment hemoglobin levels and body weight. All factors being equal, an increase in total serum cholesterol of 2.3 mmol/L was associated with a one-year prolongation of survival. After adjustment for gender, age, pretreatment cardiovascular complications, and systolic pressure, the correlations between serum cholesterol and cardiovascular and cardiac mortality were not significant.
Pulmonary arterial and venous constriction during hypoxia in 3- to 5-wk-old and adult ferrets. We have determined the sites of hypoxic vasoconstriction in ferret lungs. Lungs of five 3- to 5-wk-old and five adult ferrets were isolated and perfused with blood. Blood flow was adjusted initially to keep pulmonary arterial pressure at 20 cmH2O and left atrial and airway pressures at 6 and 8 cmH2O, respectively (zone 3). Once adjusted, flow was kept constant throughout the experiment. In each lung, pressures were measured in subpleural 20- to 50-microns-diam arterioles and venules with the micropipette servo-nulling method during normoxia (PO2 approximately 100 Torr) and hypoxia (PO2 less than 50 Torr). In normoxic adult ferret lungs, approximately 40% of total vascular resistance was in arteries, approximately 40% was in microvessels, and approximately 20% was in veins. With hypoxia, the total arteriovenous pressure drop increased by 68%. Arterial and venous pressure drops increased by 92 and 132%, respectively, with no change in microvascular pressure drop. In 3- to 5-wk-old ferret lungs, the vascular pressure profile during normoxia and the response to hypoxia were similar to those in adult lungs. We conclude that, in ferret lungs, arterial and venous resistances increase equally during hypoxia, resulting in increased microvascular pressures for fluid filtration.
P-31 spectroscopy study of response of superficial human tumors to therapy. Studies were performed to characterize phosphorus-31 magnetic resonance (MR) spectra obtained from 10 superficial human tumors outside the brain and to determine whether P-31 MR spectroscopy could allow detection of a response to therapy before a change in tumor size was measured. The ratio of phosphomonoester to adenosine triphosphate peak intensities (PME/ATP) was unusually large in all tumors studied. The average PME/ATP in lymphomas (1.8 +/- 0.5) was greater than in nonlymphoma cancers (1.1 +/- 0.15). The average PME/ATP for all tumors studied (1.4 +/- 0.5) was much greater than that of underlying skeletal muscle (0.23 +/- .09). Eight of the tumors were studied before and after therapy. Responders were distinguished from nonresponders on the basis of changes in tumor size. PME/ATP decreased during therapy in three lymphomas that responded to therapy. In an adenocarcinoma and Ewing sarcoma that did not respond to therapy, PME/ATP increased. PME/ATP remained constant in two squamous cell carcinomas that responded to therapy and decreased in one squamous cell carcinoma that decreased in size by 40% but was classified as a nonresponder. Changes in PME/ATP did not always parallel changes in tumor size during therapy. In two patients, a decrease in PME/ATP preceded a decrease in tumor size. In four patients, PME/ATP increased transiently during periods when tumor size remained constant.
Failure to detect human T-cell leukemia virus-related sequences in multiple sclerosis blood. We tested 11 patients with multiple sclerosis for the presence of human T-cell leukemia virus type I (HTLV-I)- or type II (HTLV-II)-related sequences. DNA from blood mononuclear cells was analyzed by the polymerase chain reaction utilizing three different oligonucleotide primer pairs. Two of these primer pairs detect sequences shared between HTLV-I and HTLV-II in either p24, gag protein, or in p21, env transmembrane protein. The third primer pair was synthesized based on regions in the pol gene where amino acid sequences are conserved between HTLV-I, HTLV-II, and the related bovine leukemia virus. The multiple sclerosis samples were consistently negative while appropriate control samples were positive. We conclude that viruses related to HTLV-I, HTLV-II, or bovine leukemia virus are not present in the blood of patients with multiple sclerosis and, therefore, that HTLV-bovine leukemia virus-related viruses are not likely to be involved in the pathogenesis of multiple sclerosis.
Partial laryngectomy after irradiation failure. Forty-three patients who had partial laryngectomies after radiotherapy were evaluated. Forty-two had failed irradiation for laryngeal carcinoma. Nine had supraglottic procedures, 3 endoscopic, and 31 vertical partial. Twelve (28%) required subsequent completion laryngectomy. Major complications included laryngeal stenosis in 1, incompetent laryngeal sphincters in 2, mucocutaneous fistulas in 3, and delayed deglutition in 3. Six patients had positive permanent section margins. In 5 of those, intraoperative frozen sections had been taken and were negative. Recurrent or persistent disease was eventually demonstrated in all patients with positive margins. The 2-year determinant disease-free survival rate for stage I and II disease was 85%. Three-year disease-free survival was 50% for stage III and IV disease. Partial laryngectomies, including supraglottic, can be done after irradiation failure with a high expectation of cure and acceptable morbidity. Immediate additional operation should be considered in patients with positive margins.
Regression of coronary atherosclerosis during treatment of familial hypercholesterolemia with combined drug regimens. We conducted a randomized, controlled trial in 72 patients with heterozygous familial hypercholesterolemia to test whether reducing plasma low-density lipoprotein levels by diet and combined drug regimens can induce regression of coronary lesions. Four hundred fifty-seven lesions were measured before and after a 26-month interval by computer-based quantitative angiography. The primary outcome variable was within-patient mean change in percent area stenosis. Mean low-density lipoprotein cholesterol levels decreased from 7.32 +/- 1.5 to 4.45 +/- 1.6 mmol/L. The mean change in percent area stenosis among controls was +0.80, indicating progression, while the mean change for the treatment group was -1.53, indicating regression (P = .039 by two-tailed t test for the difference between groups). Regression among women, analyzed separately, was also significant. The change in percent area stenosis was correlated with low-density lipoprotein levels on trial. We conclude that reduction of low-density lipoprotein cholesterol levels can induce regression of atherosclerotic lesions of the coronary arteries in patients with familial hypercholesterolemia. The anticipation of benefit from treatment applies to women and men alike.
Doxazosin in the treatment of mild or moderate essential hypertension: an echocardiographic study. Sixteen patients with mild or moderate essential hypertension received 1 to 8 mg/day of doxazosin (mean daily dose, 2.7 mg). Blood pressure reduction (supine and standing) was highly significant (p less than 0.001), and no significant changes in heart rate were observed. A significant reduction (p less than 0.01) in left ventricular mass was seen without a change in left ventricular systolic function. All side effects were mild, and only one patient withdrew from the study.
Should you cancel the operation when a child has an upper respiratory tract infection? Cancelling an operation when a child has an upper respiratory tract infection (URI) is not always feasible or practical. Yet we know very little about the additional risk posed by a URI occurring in a child undergoing anesthesia and surgery. Using a large prospectively collected pediatric anesthesia database, we studied 1283 children with a preoperative URI and 20,876 children without a URI. We found that children with a URI were two to seven times more likely to experience respiratory-related adverse events during the intraoperative, recovery room, and postoperative phases of their operative experience. Although these children also experienced significant disruptions in temperature regulation, they were not at risk for any other deleterious events. The elevation in risk after URI as compared with children without a URI was not explained by differences in age, physical status scores, surgical site, and emergency or elective status. However, if a child had a URI and had endotracheal anesthesia, the risk of a respiratory complication increased 11-fold (95% confidence intervals 6.8, 18.1). We conclude that the administration of general anesthesia to children with a URI is not benign and that these children require more observation/management in all perioperative phases of their surgical procedure.
A seromuscular stripping method to create a nipple valve without metal stapling for continent urinary reservoir. Urinary continence with a Kock or Mainz pouch is achieved by a nipple valve of the invaginated ileum which is usually fixed with metal staples. However, metal staples can cause various complications as a foreign body. The seromuscular stripping method, a new technique to create a nipple valve, was applied to 17 patients with bladder cancer in the construction of a continent urinary reservoir by the ileocolonic pouch (Mainz pouch). Metal staples were not used. The results were satisfactory except for 2 patients who became incontinent because of prolapse of the nipple in one and insufficient valve function due to ischemic change of the nipple valve in the other. Histology of the nipple valve from an autopsy case showed a good double layer nipple valve that functioned well to preserve continence.
Doppler echocardiographic assessment of changes in pulmonary artery pressure associated with vasodilating therapy in patients with congestive heart failure. Transpulmonic pressure gradient and pulmonary artery pressures can be estimated from the Doppler pulmonary regurgitant flow velocities by applying the simplified Bernoulli equation. In this study, continuous-wave Doppler echocardiography was used to assess changes in pulmonary regurgitant flow velocities associated with administration of vasodilators in 10 patients with congestive heart failure. M-Mode echocardiographic parameters such as left ventricular end-systolic and end-diastolic dimension and fractional shortening did not change with administration of vasodilators. Pulmonary regurgitant flow velocity at end diastole decreased from 1.9 +/- 0.6 to 1.3 +/- 0.3 m/sec (p less than 0.01), and Doppler-estimated transpulmonic pressure gradient at end diastole decreased from 16 +/- 11 to 8 +/- 4 mm Hg (p less than 0.01). Doppler-estimated transpulmonic pressure gradient at end diastole was compared with catheterization-determined pulmonary arterial end-diastolic pressure before and after administration of vasodilators in three patients, and there was a good agreement between these measurements. Thus noninvasive and sensitive assessment of the effect of vasodilators on pulmonary arterial end-diastolic pressure in patients with congestive heart failure is possible with continuous-wave Doppler echocardiographic measurement of pulmonary regurgitant flow velocities.
Aberrant origin of the right coronary artery as a potential cause of sudden death: successful anatomical correction. A man with an aberrant right coronary artery and haemodynamically important prolapse of the mitral valve was successfully resuscitated. The aberrant right coronary artery was thought to be a possible cause of the cardiopulmonary arrest in this patient. Both lesions were corrected at a single operation.
Immunophenotypes in "classical" B-cell chronic lymphocytic leukemia. Correlation with normal cellular counterpart and clinical findings. This study evaluates the expression of a series of membrane antigens, normally expressed by B-lymphocytes of the lymphocytic mantle and marginal zone, in 90 selected cases of "classical" (mouse red blood cell-receptor+, CD20+, CD5+, surface immunoglobulin +/-) B-chronic lymphocytic leukemia (B-CLL) with the aim of contributing toward identifying the normal counterpart of B-CLL and any correlations between surface antigen pattern and certain clinical characteristics. Clustered (CD23, 25, 39, 40, 27, 1c, w75) and unclustered (NuB1, 7F7, KiB3) monoclonal antibodies (MoAb) were tested. Almost all cases showed high reactivity to CD23, 27, w75, 39, 40, and NuB1: expression of CD1c was very low and that of 7F7, KiB3, and CD25 was variable. The reactivity of 7F7 and KiB3 was strictly correlated, and they correlated individually with CD25. Results show that the most frequent B-CLL phenotype (CD19+, 5+, 23+, 27+, 39+, NuB1+, KiB3 +/-, 7F7 +/-, and CD25 +/-) corresponds to one or more cellular subsets in the mantle zone. No correlation was found between MoAb expression, surface immunoglobulin (SIg) class or type, clinical stage, disease activity, or age at diagnosis. The only difference (statistically borderline) was the expression of 7F7 and KiB3 (in young versus old patients). This suggests that modulations in the expression of surface antigens do not affect the clinical behavior of the disease.
Normal and leukemic hematopoietic cells manifest differential sensitivity to inhibitory effects of c-myb antisense oligodeoxynucleotides: an in vitro study relevant to bone marrow purging. The c-myb protooncogene is preferentially expressed in hematopoietic cells, and its encoded protein, Myb, is required for hematopoietic cell proliferation. To analyze the relative Myb dependence of normal and leukemic human hematopoietic progenitor cells, normal bone marrow cells, several types of leukemic blast cells, and 1:1 mixtures of normal and leukemic cells were cultured in the presence of c-myb sense or antisense oligodeoxynucleotides; cell viability and cloning efficiency were then assessed. c-myb sense oligomers had negligible effects on normal and leukemic cells. In contrast, c-myb antisense oligomers strongly inhibited or completely abolished clonogenic growth of a T-cell leukemia line, 78% (18 of 23) of primary acute myelogenous leukemia cases examined, and 4 of 5 primary chronic myelogenous leukemia (CML) cases in blast crisis. In three of the latter patients, polymerase chain reaction analysis of a 1:1 mixture of c-myb antisense-treated normal and CML cells revealed a complete absence of bcr-abl expression, suggesting that the CML clonogenic units had been completely eliminated from the cultures. At antisense doses that inhibited leukemic cell growth, normal hematopoietic progenitor cells survived. Thus, normal and leukemic hematopoietic cells show differential sensitivity to the toxic effects of c-myb antisense DNA. Perturbation of c-myb function with antisense oligodeoxynucleotides might eventually form the basis for a molecular approach to leukemia therapy, perhaps most immediately as ex vivo bone marrow purging agents.
Treatment of ventricular tachycardia induced cardiogenic shock by percoronary chemical ablation. Incessant ventricular arrhythmias pose an especially challenging therapeutic dilemma. We describe the successful treatment and follow-up of a patient with refractory ventricular tachycardia-induced cardiogenic shock with percoronary chemical ablation. After endocardial mapping was used to identify the "tachycardia-related" coronary artery, temporary termination of the arrhythmia with balloon occlusion and subselective intracoronary installation of iced saline as previously advocated was unsuccessful. This was probably due to a dual arterial blood supply to the arrhythmogenic focus. However, infusion of 2 cc ethanol (99%) permanently terminated the arrhythmia. Contrary to previous experience, ethanol-induced arrhythmia termination did not result in arterial occlusion, further supporting a direct toxic effect on the myocardium as its mode of action. Use of standard angioplasty balloon inflation prevents "backwash" of distally infused ethanol and more generalized cell death. The only complication of this procedure was temporary third-degree AV block, requiring permanent pacemaker implantation.
Cardiorespiratory effects of endoscopic esophageal variceal sclerotherapy. Endoscopic variceal sclerotherapy (EVS) is an effective means of controlling variceal hemorrhage, which develops as a consequence of portal hypertension. While esophageal perforation, ulceration, strictures, and mediastinitis are potential complications associated with this procedure, it is not clear whether isolated pleuropulmonary events such as pleuritis, pneumonitis, and adult respiratory distress syndrome are causally related to the EVS. Endoscopy and sedation with the attendant risk of aspiration, particularly in the background of hepatic encephalopathy, may account for some of these events. Recent controlled studies of respiratory function demonstrate that EVS as such results in minor changes in gas exchange, lung volumes, and pulmonary and systemic hemodynamics. Most pulmonary complications have been reported with the use of sodium morrhuate sclerosant. Comparative studies among different sclerosants are necessary to evaluate relative safety. Finally, there have been rare reports of myocardial ischemia and pericarditis reported in association with EVS, but these are of a transient nature. Chest symptoms, roentgenographic pleuropulmonary changes, pulmonary hemodynamics, and cardiac perturbations are transient and should not preclude offering EVS to patients with variceal hemorrhage.
Growth and spread of hepatocellular carcinoma. A review of 240 consecutive autopsy cases. All 240 consecutive cases of hepatocellular carcinoma (HCC) that underwent autopsy at the National Cancer Center Hospital (Tokyo, Japan) between September 1962 and August 1986 were reviewed. Among these cases, 162, for which photographs of cut surfaces of the primary tumors were available, were grossly classified using a combination of both Eggel's classification and our own into three major types, i.e., nodular, massive, and diffuse as described by Eggel (Eggel H, Beitr Pathol Anat 1901; 30:506-604), and three subgroups of nodular type, i.e., single nodular type (type 1), single nodular type with extranodular growth (type 2), and contiguous multinodular type (type 3) by our classification (Kanai T et al., Cancer 1987; 60:810-819). Seventy-eight cases were classified as nodular type, comprising seven cases of type 1, 61 cases of type 2, and ten cases of type 3. Sixty-seven and 17 cases were classified as massive and diffuse type, respectively. Of the 78 nodular-type tumors, 59 measured less than 10 cm, whereas 64 of 67 massive-type tumors were 10 cm or more in size. The incidence of intrahepatic and extrahepatic tumor spread of HCC was significantly higher for tumors measuring more than 5 cm. As to the relationship between macroscopic type and tumor spread, the frequency of spread was lowest for type 1 tumors, and high for the other types. Intrahepatic metastasis was detected in 28.6% of type 1, 93.4% of type 2, 100% of type 3, and 98.5% of massive-type tumors. Lymph node metastasis was detected in 14.3% of type 1, 24.6% of type 2, 70% of type 3, 38.8% of massive-type and 52.9% of diffuse-type tumors. Hematogenous extrahepatic metastasis was detected in 14.3% of type 1, 47.5% of type 2, 70% of type 3, 74.6% of massive-type and 82.4% of diffuse-type tumors. It appears that not only primary tumor size but also its macroscopic type has an important influence on the growth and spread of HCC.