123rc/medical_text huggingface dataset:
Left ventricular dilatation and pulmonary thallium uptake after single-photon emission computer tomography using thallium-201 during adenosine-induced coronary hyperemia. This study examined the implications of left ventricular (LV) dilatation and increased pulmonary thallium uptake during adenosine-induced coronary hyperemia. The lung-to-heart thallium ratio in the initial images was significantly higher in patients with coronary artery disease (CAD) than normal subjects; 0.48 +/- 0.16 in 3-vessel disease (n = 16), 0.43 +/- 0.10 in 2-vessel disease (n = 20), 0.43 +/- 0.08 in 1-vessel disease (n = 16) and 0.36 +/- 0.05 in normal subjects (n = 7) (p less than 0.001, 0.09 and 0.06, respectively). There was a significant correlation between the severity and the extent of the perfusion abnormality (determined from the polar maps) and the lung-to-heart thallium ratio (r = 0.51 and 0.52, respectively, p less than 0.0002). There was also a significant correlation between lung thallium washout and lung-to-heart thallium ratio (r = 0.42, p = 0.0009) and peak heart rate (r = -0.49, p less than 0.0001). The LV dilatation was mostly due to an increase in cavity dimension (30% increase) and to a lesser extent (6% increase) due to increase in LV size. (The cavity dimensions were measured from the short-axis slices at the midventricular level in the initial and delayed images). The dilation was seen in patients with CAD but not in the normal subjects. These changes correlated with the extent and severity of the thallium perfusion abnormality. Thus, adenosine-induced coronary hyperemia may cause LV dilation and increased lung thallium uptake on the basis of subendocardial ischemia.
Interstitial chemotherapy with drug polymer implants for the treatment of recurrent gliomas. Malignant gliomas have been difficult to treat with chemotherapy. The most effective agent, BCNU (carmustine), has considerable systemic toxicity and a short half-life in serum. To obviate these problems, a method has been developed for the local sustained release of chemotherapeutic agents by their incorporation into biodegradable polymers. Implantation of the drug-impregnated polymer at the tumor site allows prolonged local exposure with minimal systemic exposure. In this Phase I-II study, 21 patients with recurrent malignant glioma were treated with BCNU released interstitially by means of a polyanhydride biodegradable polymer implant. Up to eight polymer wafers were placed in the resection cavity intraoperatively, upon completion of tumor debulking. The polymer releases the therapeutic drug for approximately 3 weeks. Three increasing concentrations of BCNU were studied; the treatment was well tolerated at all three levels. There were no adverse reactions to the BCNU wafer treatment itself. The average survival period after reoperation was 65 weeks for the first dose group, 64 weeks for the second dose group, and 32 weeks for the highest dose group. The overall mean survival time was 48 weeks from reoperation and 94 weeks from the original operation. The overall median survival times were 46 weeks postimplant and 87 weeks from initial surgery. Eighteen (86%) of 21 patients lived more than 1 year from the time of their initial diagnosis and eight (38%) of 21 patients lived more than 1 year after intracranial implantation of the polymer. Frequent hematology, blood chemistry, and urinalysis tests did not reveal any systemic effect from this interstitial chemotherapy. Since the therapy is well tolerated and safe, a placebo-controlled clinical trial has been started. The trial will measure the effect of the second treatment dose on survival of patients with recurrent malignant glioma.
Mechanism of glucoregulatory responses to stress and their deficiency in diabetes. During exercise, increased energy demands are met by increased glucose production that occurs simultaneously with the increased glucose uptake. We had previously observed that, during exercise, metabolic clearance rate of glucose (MCR) increases markedly in normal, but only marginally in poorly controlled diabetic dogs. We wished to determine (i) whether in a more general model of stress matched increases in rate of appearance of glucose and MCR also occur, or if MCR is suppressed, as during catecholamine infusion; and (ii) whether diabetes affects stress-induced changes in rate of glucose appearance and MCR. Therefore, we injected carbachol (27 nmol/50 microliters), an analog of acetylcholine, intracerebroventricularly in seven conscious dogs before and after induction of alloxan diabetes. In normal dogs, plasma epinephrine and cortisol increased 4- to 5-fold, whereas norepinephrine and glucagon doubled. Plasma insulin, however, remained unchanged. Tracer-determined hepatic glucose production increased rapidly, but transiently, by 2.5-fold. This increment can be fully explained by the observed increments in the counterregulatory hormones. Surprisingly, however, MCR also promptly increased, and therefore, plasma glucose changed only marginally. After induction of diabetes, the animals were given intracerebroventricular carbachol while plasma glucose was maintained at moderate hyperglycemia (9.0 +/- 0.4 mM). Increments in counterregulatory hormones were similar to those seen in normal dogs, except for exaggerated norepinephrine release. Peripheral insulin levels were higher in diabetic than in normal dogs; however, MCR was markedly reduced and the lipolytic response to stress increased, indicating insulin resistance. Interestingly, the hyperglycemic response to stress was 6-fold greater in diabetic than normal animals, relating mainly to the failure of MCR to rise. Plasma lactate increased equivalently in diabetic and normal animals despite suppression of MCR in the diabetics, indicating either greater muscle glycogenolysis and/or impairment in glucose oxidation. We conclude that in this stress model MCR increases as in exercise in normal but not in diabetic dogs. We speculate that glucose uptake in stress could be mediated through an insulin-dependent neural mechanism.
Intraoperative ultrasonography and the detection of liver metastases in patients with colorectal cancer. A total of 213 patients with carcinoma of the colon and rectum were examined to detect liver metastases. The study compared preoperative ultrasonography and inspection and palpation of the liver during surgery with intraoperative ultrasonography. Preoperative ultrasonography, inspection and palpation identified 238 metastases in 42 patients. Intraoperative ultrasonography detected 116 previously unrecognized metastatic tumours during 40 surgical procedures (P less than 0.01). High resolution intraoperative ultrasonography is safe and more accurate than preoperative imaging and surgical exploratory methods. The examination is simple to perform and success appears to be related to careful attention to detail.
Adult and pediatric peritonitis rates in a home dialysis program: comparison of continuous ambulatory and continuous cycling peritoneal dialysis. We reviewed our 115-month experience with continuous ambulatory peritoneal dialysis (CAPD) and continuous cycling peritoneal dialysis (CCPD) in adult and pediatric patients to determine whether there is a difference in the incidence of peritonitis between patients performing CAPD or CCPD. Peritonitis rates were similar in patients performing CAPD or CCPD in both the adult and pediatric age groups. The overall CAPD peritonitis rate was significantly lower in adult patients when compared with pediatric patients. There was no difference in peritonitis rates for CCPD between adult and pediatric patients. When the data are divided into 3-year subgroups, the incidence of peritonitis is significantly lower in adult patients undergoing either CAPD or CCPD when compared with pediatric patients during the years 1986 to 1988. There is significant improvement over time in the incidence of peritonitis in both adult and pediatric patients performing CCPD; similarly, there is a trend toward improvement in patients performing CAPD. Staphylococcus species organisms remain the most common bacterial cause of peritonitis, except in pediatric patients under the age of 2 years or with nephrostomies, where gram-negative rod infections were more common. Peritonitis resulted in discontinuation of peritoneal dialysis in a greater number of adult patients. These results suggest that the number of catheter manipulations is not important in determining the incidence of peritonitis. Pediatric patients are more likely than adult patients to develop peritonitis with either CAPD or CCPD. Adult patients are more likely than pediatric patients to discontinue peritoneal dialysis secondary to peritonitis.
The management of primary pulmonary hypertension. Primary pulmonary hypertension is a clinical syndrome characterized by pulmonary hypertension in the absence of sufficient underlying cardiac, parenchymal pulmonary, or systemic disease to account for it. The population of patients with primary pulmonary hypertension is a heterogeneous one, both clinically and histologically. As the etiologic mechanisms are unknown, therapy is directed toward the consequences of the pulmonary vascular process. Oxygen supplementation, the use of digoxin and diuretics for symptomatic heart failure, and anticoagulation all may have a role in treating primary pulmonary hypertension, although vasodilator therapy has been the main area of investigation. Screening for vasodilator responsiveness, defining a favorable vasodilator effect, predicting long-term effectiveness, and deciding who to treat have all been controversial. New approaches, such as use of high-dose calcium channel-blocking agents and continuous intravenous infusion of prostacyclin (an investigational agent), have recently been proposed. When medical therapies are exhausted, heart-lung or lung transplantation has increasingly become an option for selected patients.
Physiologic peripheral pulmonic stenosis in infancy. We studied 14 premature infants with the clinical diagnosis of peripheral pulmonic stenosis (PPS) and 15 normal full-term neonates by echocardiographic Doppler examinations. The PPS group had an average main pulmonary artery (PA) diameter similar to the control group (0.91 vs 0.96 cm, difference not significant), but had smaller branch PA diameters: right PA = 0.41 vs 0.50 cm, p less than 0.001, and left PA = 0.41 vs 0.49 cm, p less than 0.001. The PPS group also had greater peak velocities in the main PA (76 vs 63 cm/s, p less than 0.05), right PA (193 vs 118 cm/s, p less than 0.001) and left PA (187 vs 123 cm/s, p less than 0.001). Similarly, the ratio of peak velocity in the branch/main PA was greater for the PPS group: right/main PA peak velocity = 2.91 vs 1.92, p less than 0.01, and left/main PA peak velocity = 2.73 vs 1.99, p less than 0.05. The calculated right ventricular output for the PPS group was more than the control group: 437 vs 261 ml/min/kg, p less than 0.001. Hematocrits were not done on the control group, but the PPS group had an average hematocrit which was low (34%). It is concluded that patients with PPS have mild underdevelopment of the PA branches, with consequent increased flow velocity and turbulent flow. This turbulent flow may be contributed to by increased cardiac output and mild anemia.
Inflammatory bowel disease and tobacco smoke--a case-control study. A case-control study was carried out in Stockholm, Sweden between 1984 and 1987 to evaluate the association of cigarette smoking and exposure to environmental tobacco smoke during childhood and the subsequent development of inflammatory bowel disease. Information on smoking was obtained by a postal questionnaire. The relative risk of Crohn's disease in current smokers compared with those who had never smoked was 1.33 (95% confidence limits 0.7; 2.6) in men and 4.99 (2.7; 9.2) in women; the corresponding results for ulcerative colitis were 0.96 (0.5; 1.8) and 0.72 (0.4; 1.4). The relative risk of ulcerative colitis in recent exsmokers compared with those who had never smoked was 2.18 (0.9; 5.0). Furthermore, an increase in the risk of Crohn's disease was found in those who were exposed to environmental tobacco smoke during childhood, the relative risk being 1.50 (1.0; 2.3). The corresponding relative risk of ulcerative colitis was 0.98 (0.6; 1.5).
The relationship of prostate specific antigen levels and residual tumor volume in stage A prostate cancer. Preoperative serum prostate specific antigen correlates well with morphometrically determined prostate tumor volume in prostatectomy specimens. However, since prostate specific antigen is produced by hyperplastic as well as malignant prostatic epithelium, the contribution of hyperplastic epithelium (benign prostatic hyperplasia) to serum prostate specific antigen interferes with the ability of serum prostate specific antigen to predict tumor volume in individual patients. We wondered if the removal of benign prostatic hyperplasia tissue would increase the correlation between prostate specific antigen and tumor volume, and, thus, make prostate specific antigen a more accurate predictor of residual cancer volume after transurethral resection of the prostate. A total of 67 patients with clinical stage A cancer underwent radical retropubic prostatectomy (22, or 33%, with stage A1 and 45, or 67%, with stage A2 disease), and had pre-radical prostatectomy measurement of serum prostate specific antigen and morphometric determination of residual cancer volume in the radical prostatectomy specimen. The correlation between serum prostate specific antigen and residual cancer volume for all 67 patients was 0.66, and for stages A1 and A2 disease it was 0.64 and 0.70, respectively. All stage A1 cancer patients with a serum prostate specific antigen value of 1 ng./ml. or less had residual tumor volumes of less than 0.5 cc and all stage A cancer patients with a serum prostate specific antigen value of more than 10 ng./ml. had residual tumor volumes of greater than 0.5 cc. Of the patients 51% had levels of 1 to 10 ng./ml. and serum prostate specific antigen was not useful to predict residual tumor volume in this group. Serum prostate specific antigen measurements may be helpful in stage A1 cancer patients with levels of 1 ng./ml. or less, or greater than 10 ng./ml. in choosing the most appropriate therapy.
Mast cell/nerve interactions in vitro and in vivo. In this report, we review the evidence for mast cell/nerve interactions. We believe that the morphologic and functional evidence now strongly support a purposeful and biologically significant interaction between these two cell types. This interaction has physiologic consequences and appears to be able to regulate such local events as chloride ion secretion by epithelial cells of the intestinal and respiratory tracts in experimental models. In this way, the mast cell and nerve may be considered as a functional homeostatic regulatory unit. The extent to which this unit may be involved in maintenance of normal integrity of mucous membranes or other structures, in health and in disease, is not clear at the present and will require considerably more investigation and elucidation. However, the concept of such an interaction is an interesting one and may bring new approaches of a therapeutic and diagnostic nature to bear on some old problems. The observations reviewed in this report that psychologic conditioning may itself cause mucosal mast cell degranulation and mediator release in the rat is significant. We consider that this evidence of central nervous system control of mast cell degranulation is an extension of the idea that mast cells and nerves communicate.
Thyroid and parathyroid cancer. The epidemiology, etiology, pathology, and management of thyroid and parathyroid carcinoma are discussed. Emphasis is placed on the clinical differences in the management and treatment of the various histologic subtypes of thyroid cancer. The biologic and prognostic differences among the various histologic types of thyroid cancer and their relationship to age are stressed.
Differential effects of sodium butyrate and hexamethylene bisacetamide on growth and secretion of cultured human endocrine tumor cells. Advanced gastrointestinal endocrine tumors respond poorly to conventional chemotherapy. In this study we examined the effects of two agents that promote cellular differentiation, sodium butyrate and hexamethylene bisacetamide, on the in vitro growth and secretory responses of a human pancreatic carcinoid (BON) and human gastrinoma (PT-2 and PT-SM) cell lines that have been established in our laboratory. We found that both sodium butyrate and hexamethylene bisacetamide strongly inhibited growth of BON, PT-2, and PT-SM cells. With continuous exposure of BON cells to sodium butyrate (2 mmol/L), the doubling time was prolonged, from 60 hours in controls to 156 hours, and saturation density was reduced to 28% that of controls. Hexamethylene bisacetamide (4 mmol/L) reduced saturation density to 37% that of controls in BON cells and prolonged the doubling time, from 60 hours to 103 hours. Antiproliferative effects of similar magnitudes were observed in the gastrinoma cell lines. In contrast, differential effects were produced on amine biosynthesis in BON cells; sodium butyrate stimulated levels of 5-hydroxytryptamine in the cells, whereas hexamethylene bisacetamide caused a profound dose-dependent inhibition of amine biosynthesis. The significant antiproliferative activity of sodium butyrate and hexamethylene bisacetamide and the inhibitory effects of hexamethylene bisacetamide on amine biosynthesis warrant evaluation of these agents or analogues for treatment of metastatic carcinoid and gastrinoma.
Myocardial uptake of indium-111-labeled antimyosin in acute subendocardial infarction: clinical, histochemical, and autoradiographic correlation of myocardial necrosis. Indium-111-labeled antimyosin has been utilized in the diagnosis and localization of acute transmural myocardial infarction. The present report describes a patient who presented with a massive subendocardial infarction. Two days after the injection of antimyosin, the patient's clinical status markedly deteriorated and he expired. Postmortem examination demonstrated severe three-vessel coronary artery disease with extensive myocyte death in the endocardium. Autoradiography and histochemical staining of the prosected heart demonstrated high correlation for myocardial necrosis and corresponded to clinical evidence for diffuse subendocardial infarction.
A 3-bp deletion in the rhodopsin gene in a family with autosomal dominant retinitis pigmentosa. Autosomal dominant retinitis pigmentosa (ADRP) has recently been linked to locus D3S47 (probe C17), with no recombination, in a single large Irish family. Other ADRP pedigrees have shown linkage at zero recombination, linkage with recombination, and no linkage, demonstrating genetic heterogeneity. The gene encoding rhodopsin, the rod photoreceptor pigment, is closely linked to locus D3S47 on chromosome 3q. A point mutation changing a conserved proline to histidine in the 23d codon of the gene has been demonstrated in affected members of one ADRP family and in 17 of 148 unrelated ADRP patients. We have sequenced the rhodopsin gene in a C17-linked ADRP family and have identified in the 4th exon and in-frame 3-bp deletion which deletes one of the two isoleucine monomers at codons 255 and 256. This mutation was not found in 30 other unrelated ADRP families. The deletion has arisen in the sequence TCATCATCAT, deleting one of a run of three x 3-bp repeats. The mechanism by which this occurred may be similar to that which creates length variation in so-called mini- and microsatellites. Thus ADRP is an extremely heterogeneous disorder which can result from a range of defects in rhodopsin and which can have a locus or loci elsewhere in the genome.
A simple score for the identification of patients at high risk of organic diseases of the colon in the family doctor consulting room. The Local IBS Study Group. In order to develop a scoring system for selecting patients at high risk of organic diseases of the colon, who would need a colonoscopy or a barium enema, we conducted a study with 14 GPs in the local health care district of Modena. Over one year, 254 consecutive patients who consulted their GP for chronic abdominal pain were asked to answer a guided questionnaire. A checklist of simple parameters suggestive of the presence of organic diseases of the colon was also registered by the GP. For the final diagnosis, the patients underwent either a colonoscopy or a barium enema. Data collected were analysed by means of a stepwise logistic regression analysis to obtain a weighted score for the diagnosis of either irritable bowel syndrome (score less than 0) or organic disease (score greater than 0). Out of the 25 parameters explored, six were significantly more common among patients with organic disease and weighted as positive score (namely ESR greater than 17 mm, first hour, history of blood in the stool, leukocytosis greater than 10,000 cm3, age greater than 45 years, slight fever and presence of neoplastic colonic diseases in first-degree relatives). On the contrary, five parameters were more frequent among patients with irritable bowel syndrome and weighted as negative score (namely visible distension of the abdomen, feeling of distension, presence of irritable bowel syndrome in first degree relatives, flatulence and irregularities of bowel movement). Our scoring system correctly classified 83.5% of the cases, and it was very sensitive (82.4%) for the diagnosis of organic disease.
Hydatid cyst of the interatrial and interventricular septum of the heart. To our knowledge this report describes the first case of a large hydatid cyst involving the full thickness of both the interatrial and interventricular septum of the heart, which was detected at autopsy. The cyst was intact. Clinically, there was complete heart block.
Ventricular arrhythmias in hypertensive left ventricular hypertrophy. Relationship to coronary artery disease, left ventricular dysfunction, and myocardial fibrosis. Ventricular arrhythmias occur with increased frequency in hypertensive patients with left ventricular hypertrophy (LVH). The relationships, however, between ventricular arrhythmias and coexistent coronary artery disease, left ventricular dysfunction and left ventricular fibrosis have not been examined in hypertensive LVH. We carried out coronary arteriography on fifteen hypertensive patients with LVH and nonsustained ventricular tachycardia (greater than or equal to 3 consecutive ventricular complexes) of whom nine (60%) were free of significant (greater than 50% stenosis) coronary disease. To identify other possible correlates of left ventricular arrhythmias, 28 patients with LVH, comprising 17 with ventricular tachycardia and 11 without ventricular arrhythmias, underwent quantitative assessment of left ventricular function (angiographic ejection fraction), left ventricular mass (echocardiography), and left ventricular fibrosis (endomyocardial biopsy). Ejection fraction was not significantly different between the two groups (53 +/- 8% v 62 +/- 2%, P = NS). However, left ventricular mass was significantly greater (442 +/- 28 g v 339 +/- 34 g, P less than .05) and percentage fibrosis significantly higher (19 +/- 4% v 3 +/- 1%, P less than .001) in those patients with ventricular tachycardia. Thus ventricular arrhythmias in hypertensive patients with LVH cannot be entirely attributed to coexistent coronary disease, nor to left ventricular dysfunction, but are related to the degree of cardiac hypertrophy and subendocardial fibrosis.