shukoor65/lab-rag-model huggingface dataset:
Abdominal desmoids: CT findings in 25 patients. Desmoids are histologically benign but locally aggressive fibrous tumors. Although overall they are rare lesions, they are a common manifestation of Gardner syndrome. We retrospectively reviewed clinical records and CT scans of 25 patients with abdominal desmoids. The number, location, and CT characteristics of the lesions were recorded for each patient. Tumors were solitary in 72% of patients and multiple in 28%. Fifty percent were located in the abdominal wall, 41% in the mesentery, and 9% in the retroperitoneum. More than two thirds of the lesions had well-defined borders, with the remainder displaying an infiltrative outer margin. The majority of tumors had attenuation values equal to (47%) or greater than (41%) the attenuation of muscle on contrast-enhanced CT scans. Complications attributable to the desmoid were commonly detectable on CT (hydronephrosis occurred in 36% and small-bowel obstruction in 20%). Our results detail the spectrum of CT findings and complications caused by abdominal desmoids.
Adrenaline injection for endoscopic haemostasis in non-variceal upper gastrointestinal haemorrhage. Over a 30-month period, 53 patients with actively bleeding non-variceal lesions of the oesophagus, stomach or duodenum were treated by endoscopic injection of 1/10,000 adrenaline. Initial haemostasis was obtained in 50 cases, and permanent haemostasis in 44. Emergency surgery for bleeding was required in nine patients overall, and there were four deaths. All lesions requiring surgery were located on the posterior wall of the duodenum or the lesser curve of the stomach, and all but one had evidence of an exposed arterial vessel. Adrenaline injection is an effective, safe and simple method of endoscopic haemostasis.
Professional mammographic quality assessment program for a community hospital. The evaluation of mammographic interpretations is a difficult challenge for a professional quality assessment program. As most images are read by a single observer and pathologic proof is obtained only if prompted by the report or if clinical symptoms warrant surgical intervention, it is difficult to construct a meaningful quality assessment program. The authors designed a program on the basis of a mammographic coding system that allows both individual physicians and practice groups to be evaluated. The program examines mammographic reports to determine the consistency of reporting by each physician and by the entire group. In addition, the program facilitated periodic evaluation of physicians with use of test cases. The coding system provided an easy method of correlating the mammographic reports with pathology reports from biopsy specimens, allowing a more thorough examination of possible systematic errors in the evaluation of the examinations, as well as enabling calculation of the positive predictive value for the diagnosis of cancer. The professional quality assessment program can be easily implemented in a busy clinical setting to evaluate whether mammograms were read consistently and "correctly" and to provide a method of continuing education for the physicians.
Malignant fibrous histiocytoma of the gastrointestinal tract in a patient with neurofibromatosis. Malignant fibrous histiocytoma (MFH) of the gastrointestinal tract is extremely rare. A case of MFH of the colon associated with neurofibromatosis is presented. MFH is a high-grade soft-tissue sarcoma of fibroblast cell origin with a strong propensity for metastasis and recurrence. Immunochemical markers help to differentiate MFH from other sarcomas. The most successful treatment of MFH is surgical extirpation. Adjuvant chemotherapy and radiotherapy have not been definitively shown to be of value.
Clinical follow-up and progression of carotid atherosclerosis determined by duplex scanning in patients suffering from TIA. We investigated the clinical outcomes and the progression of the internal carotid arterial lesions of a group of patients presenting with hemispheric TIAs. The cumulative frequency of TIAs during a mean follow-up period of 40 +/- 14 months was 14%, and no relationship was found between new TIAs and the presence of known cardiovascular risk factors or plaque characteristics as determined by duplex scanning. With the exception of one patient who died of stroke, none of the patients developed a permanent neurologic deficit. The cumulative death rate was 6.5%; myocardial infarction was the most common cause (3 out of 7). Anatomic progression of plaques was determined by duplex scanning in 22% of the internal carotid arteries. No relationship between progression of these plaques and the development of new TIAs was evident. We conclude that, in this group of patients, TIAs do not inevitably lead to stroke and that TIAs are not predictable based on risk factors or plaques characteristics.
Limb salvage surgery for bone and soft tissue sarcoma. A phase II pathologic study of preoperative intraarterial cisplatin. Preoperative therapy has been tested as part of limb salvage therapy for localized bone and soft tissue sarcoma of the extremities. The activity of cisplatin (CDDP) by intraarterial (IA) infusion was evaluated in 40 cases of which 36 were evaluable for response. All patients had high-grade sarcomas. All but 3 patients received 3 or 4 courses (24 patients received 4 courses) of CDDP at a dosage of 120 to 150 mg/m2 given over 6 hours every 2 weeks by IA infusion. Patients younger than 18 years of age received the higher dose of CDDP. Treatment was well tolerated with combination antiemetics. One patient experienced severe hearing loss with the first cycle of the higher CDDP dose. Pathologic evaluation of resected osteosarcoma showed a favorable response (90% or greater necrosis) in 8 of 20 evaluable cases and in 3 of 4 patients with malignant fibrous histiocytoma (MFH) of bone (without osteoid). In soft tissue sarcomas, minimal (50% to 89%) necrosis was seen in two of nine cases and none had 90% or greater necrosis. Patients received postoperative chemotherapy based on pathologic response, but the value of this postoperative adjuvant therapy requires further follow-up and is uncertain in this small study. IA CDDP can often cause significant tumor necrosis in patients with bone sarcomas, whereas soft tissue sarcomas are less sensitive to this therapy.
Endogenous opiates modulate the postapnea ventilatory response in the obstructive sleep apnea syndrome. Defense of ventilatory homeostasis against recurrent hypercapnia, hypoxia, and acidosis resulting from apnea in obstructive sleep apnea syndrome (OSAS) is dependent on compensatory mechanisms operative between episodes of airway obstruction. This investigation was designed to examine whether endogenous opiate activity modulates the compensatory ventilatory response to apnea in OSAS. Polysomnography and quantitative measurement of tidal volume was performed in 12 patients with moderate to severe OSAS during a morning nap study before and after intravenous administration of 10 mg of naloxone. Apnea index was not significantly altered. There was a small but significant shortening of apneas (postnaloxone apnea duration, 91.2% of prenaloxone; p = 0.002 by ANOVA). Tidal volume of the first postapnea breath and minute ventilation extrapolated from the first two postapnea breaths, but not frequency, increased significantly after naloxone (postnaloxone first breath volume, 112.7% of prenaloxone value [p = 0.03], with a similar increase for minute ventilation, 115.1% [p = 0.007]). The volume of the first postapnea breath was correlated with the duration of the previous apnea, both before (r = 0.59, p = 0.0001) and after naloxone. Despite this, analysis of covariance with apnea duration as the covariate confirmed a significant independent increase in postapnea breath volume after naloxone (p = 0.001). Naloxone also altered sleep architecture, increasing percent time awake during the study period (prenaloxone, 36.3 +/- 15.6%; postnaloxone, 56.7 +/- 22.4%; p = 0.0003) and decreasing total sleep time and percent time in Stage 1. Furthermore, naloxone increased continuity of awake periods (mean length of awake periods increased from 27.0 +/- 8.4 to 66.0 +/- 66.6 s after naloxone, p = 0.05).
Radiographic fallopian tube recanalization: absorbed ovarian radiation dose. Absorbed radiation dose to the ovaries during radiographic fallopian tube recanalization was estimated in 29 patients with use of thermoluminescent dosimeters placed in the vaginal fornix. With an average fluoroscopic time of 8.5 minutes +/- 5.5 and an average of 14 +/- 5 105-mm spot radiographs obtained, the average absorbed dose to the ovaries was 8.5 mGy +/- 5.6 (0.85 rad +/- 0.56). Technical guidelines for keeping patient radiation exposure to a minimum during this new interventional procedure are suggested.
Patterns of failure in Hancock pericardial bioprostheses. A series of Hancock pericardial valve bioprostheses was reviewed for cases of primary valve failure. Thirteen mitral and 10 aortic valve explants were recovered from 21 adult patients. Mitral valves had been in place for a mean of 56.4 months, and aortic valves for 53.8 months. All valves failed with cusp tears from stents (with a mean of 1.7 for mitral valves and 2.6 for aortic valves) in a predictable pattern, suggesting that wear and stress at cusp stitch sites are important in their pathogenesis. The topography of these tears is illustrated as are the less common associates of primary failure, such as calcification, fibrosis, and thrombosis. Similarities and differences of this valve's failure compared with that of the Ionescu-Shiley pericardial valve are discussed.
Left bronchial isomerism associated with bronchomalacia, presenting with intractable wheeze. The cause of the Williams Campbell syndrome (bronchomalacia with bronchiectasis) is controversial. A boy with bronchomalacia, bifid ribs, and left bronchial isomerism presented with intractable wheeze mimicking asthma. The combination of the abdominal, bronchial, and atrial anatomy seen in this child has been described only once previously. The coexistence of these congenital abnormalities in this boy supports a congenital cause for the Williams Campbell syndrome. The need to assess wheezy children critically is emphasised.
Rapid thrombus dissolution by continuous infusion of urokinase through an intracoronary perfusion wire prior to and following PTCA: results in native coronaries and patent saphenous vein grafts. Even with aspirin and heparin therapy, thrombus present prior to or forming after percutaneous transluminal coronary angioplasty (PTCA) results in significant complications. We report on 33 patients who were treated with continuous infusion of Urokinase through an intracoronary perfusion wire for 24 hr because of visible intracoronary thrombus. Seventeen native vessels (9 pre-PTCA and 8 post-PTCA) and sixteen saphenous vein grafts (12 pre-PTCA and 4 post-PTCA) were treated. All vessels were patent at the time of perfusion wire placement. Complete thrombus resolution, successful PTCA and sustained patency was seen in 31 of 33 patients. One native vessel treated post PTCA (originally occluded) re-occluded. One saphenous vein graft treated prior to PTCA showed improvement in thrombus but distal embolization with balloon inflation occurred. No significant complications related to the intracoronary infusion technique were observed. In conclusion, rapid lysis of intra-coronary thrombus can be accomplish safely using this technique and can result in improved PTCA outcome.
Surgical treatment of the Wolff-Parkinson-White syndrome by epicardial electrical ablation A new operation to eliminate accessory pathways--epicardial electrical ablation--is described. In a group of 201 patients without concomitant disease, the mortality rate was 0.5% and the overall efficacy of the operation for free wall accessory pathways, 98%. A retrospective clinical study of 44 unselected patients was performed to examine how safe epicardial electrical ablation is. The criteria for intraoperative effectiveness were disappearance of both the delta wave and retrograde conduction and inability to induce tachycardia. In the postoperative and follow-up periods, the following were reviewed: electrocardiograms; Holter monitor recordings (24 to 26 hours); release of the myocardial-specific isoenzyme of creatine kinase; intracardiac hemodynamics and myocardial contractility (radionuclide methods); selective coronary arteriograms and ventriculograms; mean work capacity (bicycle ergometer); diagnostic transesophageal electrical stimulation; and histology of the area of ablation. The main conclusion of this study is that epicardial electrical ablation is a highly efficient and safe operation for surgical elimination of parietal accessory pathways in patients with Wolff-Parkinson-White syndrome. Its advantages are its technical simplicity and the opportunity to review results immediately during the operation.
Relationship between insulin sensitivity, insulin secretion and glucose tolerance in cirrhosis. Hepatic insulin extraction is difficult to measure in humans; as a result, the interrelationship between defective insulin secretion and insulin insensitivity in the pathogenesis of glucose intolerance in cirrhosis remains unclear. To reassess this we used recombinant human C-peptide to measure C-peptide clearance in cirrhotic patients and controls and thus derive C-peptide and insulin secretion rates after a 75-gm oral glucose load and during a 10 mmol/L hyperglycemic clamp. Cirrhotic patients were confirmed as insulin-insensitive during a euglycemic clamp (glucose requirement: 4.1 +/- 0.1 mg/kg/min vs. 8.1 +/- 0.5 mg/kg/min; p less than 0.001), which also demonstrated a low insulin metabolic clearance rate (p less than 0.001). Although intolerant after oral glucose, the cirrhotic patients had glucose requirements identical to those of controls during the hyperglycemic clamp (cirrhotic patients: 6.1 +/- 1.0 mg/kg/min; controls: 6.3 +/- 0.7 mg/kg/min), suggesting normal intravenous glucose tolerance. C-peptide MCR was identical in cirrhotic patients (2.93 +/- 0.16 ml/min/kg) and controls (2.96 +/- 0.24 ml/min/kg). Insulin secretion was higher in cirrhotic patients, both fasting (2.13 +/- 0.26 U/hr vs. 1.09 +/- 0.10 U/hr; p less than 0.001) and from min 30 to 90 of the hyperglycemic clamp (5.22 +/- 0.70 U/hr vs. 2.85 +/- 0.22 U/hr; p less than 0.001). However, with oral glucose the rise in serum C-peptide concentration was relatively delayed, and the insulin secretion index (secretion/area under 3-hr glucose curve) was not elevated. Hepatic insulin extraction was reduced both in fasting and during the hyperglycemic clamp (p less than 0.001).
Platelet-activating factor in stroke and brain injury. Platelet-activating factor, an endogenous phospholipid of proinflammatory, hemostatic, and vasoactive properties, is synthesized by neurons and in injured brain. Platelet-activating factor is released together with eicosanoids such as thromboxane A2, prostacyclin, and leukotrienes. Its effects in neurons are mediated through a specific receptor coupled to phospholipase C and phosphoinositol metabolism. The cerebrovascular effects of platelet-activating factor include disruption of the blood-brain barrier, edema formation, and vasospasm. It has also been described to possess direct toxicity to neuronal cells in culture. Discovery and development of several highly potent and selective antagonists to platelet-activating factor receptors facilitated experimental studies underscoring the role of this factor as an endogenous mediator in cerebral disorders, particularly cerebral ischemia and trauma. Significant biochemical, microvascular, functional, and behavioral recovery has been demonstrated using these antagonists in an array of experimental models of focal and global ischemia in the central nervous system (CNS). Clearly, studies of platelet-activating factor in experimental models of CNS ischemia and reperfusion injury open a new perspective on phospholipid metabolism in stroke and offer an exceptionally promising therapeutic prospect. Data supporting this factor as a mediator of specific pathological sequelae in stroke and neuroinjury are surveyed in this review. We discuss the mechanisms and significance of platelet-activating factor-mediated effects and propose directions for future studies.
Hypertension as a causative diagnosis of patients entering end-stage renal disease programs in the United States from 1980 to 1986. Treatment of hypertension has decreased the incidence of stroke and congestive heart failure consequential to hypertension. To determine whether the incidence of hypertension as a causative diagnosis of end-stage renal disease (ESRD) is also decreasing, we examined the records of the Health Care Financing Administration (HCFA) from 1980 to 1986 regarding the causative diagnoses of patients entering ESRD programs. We found that the incidence of patients entering ESRD programs increased during the study period. Hypertension as a causative diagnosis was a constant proportion of the increase. The greatest increase occurred in patients age 55 or more years. This was strikingly true of black patients. We conclude that there has not been a decrease in the incidence of hypertension as a causative diagnosis for patients entering ESRD programs and that this may be a reflection that treatment of hypertension does not prevent the development of ESRD in some patients. We propose that prospective studies be undertaken to determine whether this is the case.
Hyperthyroidism due to a pituitary adenoma composed of two different cell types, one secreting alpha-subunit alone and another cosecreting alpha-subunit and thyrotropin. A 37-yr-old female presented with clinical signs and symptoms of mild hyperthyroidism, high serum levels of free T4 (24.2 pmol/L), free T3 (11.7 pmol/L), and sex hormone-binding globulin (157 nmol/L) as well as measurable (by immunofluorometric assay) serum TSH concentrations (1.9 mU/L) in the absence of any known methodological interference. The above finding indicated the presence of hyperthyroidism due to inappropriate secretion of TSH, whose neoplastic origin was documented by computed tomographic scan showing a 1-cm pituitary adenoma. The diagnosis was confirmed by elevated alpha-subunit levels (9.2 micrograms/L) and alpha-subunit/TSH molar ratio (25.2) as well as absent TSH suppression after T3 administration. TRH injection (200 microgram, iv) caused impaired TSH (from 3.0 to 4.8 mU/L) and unexpectedly exaggerated alpha-subunit (from 8.8 to 18.2 micrograms/L) responses. Such a discrepancy was also observed after other dynamic tests. Double gold particle immunostaining of the adenomatous tissue removed at surgery showed that all of the cells contained secretory granules positive for alpha-subunit, while very few cells were positive for TSH beta and alpha-subunit. In conclusion, the present study demonstrates the existence of TSH-induced hyperthyroidism due to a pituitary adenoma composed of two different cell types: one secreting alpha-subunit alone and another cosecreting alpha-subunit and TSH.
Evaluation of valvular heart disease with cine gradient echo magnetic resonance imaging. Electrocardiographic referenced repetitive gradient echo magnetic resonance imaging (cine GRE) has been used to detect and quantify valvular regurgitation. Regurgitation is recognized as a signal void in the high intensity blood pool on these images. Mitral regurgitation causes a signal void in the left atrium in systole, and aortic regurgitation produces one in the left ventricle in diastole. The specificity, sensitivity, and diagnostic accuracy of cine GRE for the detection of mitral and aortic regurgitation was greater than 0.93, 0.89, and 0.92, respectively. The severity of regurgitation has been quantified as the difference in the stroke volume between the two ventricles by measuring the volume of the blood pool, as shown in the stack of magnetic resonance tomograms. Severity has also been assessed by measuring the volume of the signal void. Finally, measurements of the volume of aortic regurgitation have recently been achieved by using velocity-encoded cine GRE. This technique provides a direct measurement of retrograde flow in the aorta during diastole. New cine GRE imaging techniques provide a noninvasive means for quantification of valvular as well as ventricular function.
Cerebral haemorrhage in a French prospective population study. The incidence of cerebral haemorrhage was studied from a population-based stroke registry. The incidence was 12.3 per 100,000 per year in women and 13.9 per 100,000 per year in men, with a peak in the eighth decade and a male preponderance. Haemorrhages were deep seated and mostly due to hypertension. Recognised clinical characteristics of haemorrhage are acute onset, convulsion, vomiting, and disturbed consciousness. This study showed that cerebral haemorrhage may present with pure motor deficit or transient deficit preceding the stroke. The mortality was 51% in the first month, and 61% by two years.
Cellular intermediate filament networks and their derangement in alcoholic hepatitis. Intermediate filaments are major components of most eukaryotic cells that form from the polymerization of protein subunits that are expressed in tissue and development specific fashions. The interactions of intermediate filaments with a myriad of other cellular proteins and structures give rise to a complex overall cellular architecture that is likely responsible for cellular well-being. The mature 10-nm filaments are relatively stable cellular structures, but the intermediate filaments undergo major morphological and biochemical changes, especially during mitosis, differentiation, and in response to certain drugs. Evidence exists that hepatocyte intermediate filaments (keratin filaments) are deranged in alcoholic hepatitis, an inflammatory liver disease of alcoholics and heavy spree drinkers. The classical and characteristic pathological hepatocyte inclusion bodies of alcoholic hepatitis, Mallory bodies, are composed in part of normal keratins that likely derive from the pre-existing hepatocyte intermediate filament network. It is unclear if intermediate filament network derangement in alcoholic hepatitis is directly caused by the actions of ethanol or its metabolites on intermediate filaments or their associated structures, or whether alcohol causes a cellular insult or injury elsewhere and a subsequent response (e.g., immune) causes intermediate filament network derangement. The precise mechanisms responsible for intermediate filament derangement remain to be elucidated; however, experimental data exist that support and refute several hypotheses. Hopefully, further studies will help determine a better overall understanding of the abnormalities of intermediate filaments and their relationship to the pathophysiology of alcoholic hepatitis and other diseases.
Pleuropulmonary complications of endoscopic variceal sclerotherapy. The most common pulmonary complication of EVS is pleural effusion. The most clinically significant pulmonary complication of EVS is delayed perforation with formation of esophagopleural or esophagobronchial fistula. Pneumonia, empyema, pulmonary infarction, and atelectasis can also occur. Endoscopic variceal sclerotherapy probably does not cause ARDS, but that issue remains unsettled. Transient relative pulmonary hypertension during EVS is probably of no clinical significance, but caution is urged when sclerosing varices in a patient with borderline right heart function.
An unusual problem during surgical removal of a broken guidewire. At operation, it proved impossible using traction alone to remove an angioplasty guidewire that was lodged in an intermediate artery. The problem was solved by passing a Teflon catheter over the wire, thus protecting the left main coronary artery while freeing the entrapped distal end of the guidewire.