shukoor65/lab-rag-model huggingface dataset:
Routine histological compared with immunohistological examination of bone marrow trephine biopsy specimens in disseminated neuroblastoma. The ability to detect infiltration in bone marrow biopsy specimens from patients with disseminated neuroblastoma was assessed by immunohistological and routine histological methods. Frozen cores from 33 staging procedures were tested with UJ13A and UJ127.11. Immunopositive tumour cells were found in 10 of 17 staging procedures in which tumour was detectable by routine histological methods. Positive cells or stromal material were also found in eight of 12 staging procedures in which distorted architecture and fibrosis, but no obvious tumour, had been noted. Paraffin wax embedded cores from 29 of the same staging procedures were tested with antibodies against neurone specific enolase and neurofilament. Only a single core reacted with anti-neurofilament antibody. Neurone specific enolase positive cells or stromal material were found in nine of 15 staging procedures in which obvious tumour was detectable. Although these immunohistochemical techniques proved inferior to routine histology in their ability to detect obvious tumour, the demonstration of immunopositive stromal tissue which was not frankly malignant supports the view that distorted, fibrotic marrow may reflect persistence of neuroectodermal tissue and justifies its distinction from normal marrow when reporting the response to treatment.
Clinical, radiographic, and histologic study of endodontic treatment failures. One hundred fifty cases of endodontic treatment failures were studied clinically, radiographically, and histologically. Fifty-seven percent of the teeth were asymptomatic. Pain alone and/or associated with swelling was present in 21% of the teeth. There was no correlation between the size of periradicular rarefaction and the occurrence or severity of clinical signs and/or symptoms. Stainable bacteria were demonstrated in 69% of the teeth and were present mostly in the canal. The severity of periradicular inflammation was related to presence of stainable bacteria in the canal. Swelling and pain or a draining sinus tract was often associated with stainable bacteria inside the canal. The development of a radicular cyst associated with an endodontically treated tooth that has failed is not necessarily the cause of endodontic treatment failure.
Cardiopulmonary resuscitation of apparently stillborn infants: survival and long-term outcome. To determine the outcome of apparently stillborn infants who received cardiopulmonary resuscitation, we studied the short- and long-term outcome of 93 infants who had an Apgar score of 0 at 1 minute of age and were resuscitated at birth. Sixty-two (66.6%) responded and left the delivery room alive; 26 (42%) of the 62 infants died in the neonatal period and 36 infants were discharged home; of the 36 infants, three subsequently died during infancy. Of the 33 survivors, ten were lost to follow-up after discharge. Developmental assessment of 23 of 33 long-term survivors revealed normal outcome in 14 (61.7%), abnormal results in 6 (26%), and suspect status in 3 (13%). Fifty-eight infants had an Apgar score of 0 at greater than or equal to 10 minutes of age and all except one died; the surviving infant has an abnormal developmental outcome. We conclude that 39% of apparently stillborn infants who were resuscitated survived beyond the neonatal period and that 61% of the 23 survivors who were available for developmental follow-up had normal development at the time of last examination. Survival was unlikely if there was no response after 10 minutes of resuscitation.
Blood transfusion and oxygen consumption in surgical sepsis. OBJECTIVE: To evaluate the use of serum lactic acid values to predict flow-dependent increases in oxygen consumption (VO2) in response to increasing oxygen delivery (DO2) after blood transfusion in surgical sepsis. DESIGN: Prospective study. SETTING: Tertiary care, trauma center. PATIENTS: Twenty-one patients, postsurgical or posttrauma, judged septic by defined criteria. INTERVENTIONS: Serum lactic acid concentrations, DO2, and VO2 were measured before and after transfusion therapy. MEASUREMENTS AND MAIN RESULTS: Overall, the DO2 increased from 532 +/- 146 to 634 +/- 225 (SD) mL/min.m2 (p less than .001), and the VO2 increased from 145 +/- 39 to 160 +/- 56 mL/min.m2 (p = .02). These changes occurred with an Hgb increase from 9.3 +/- 1.1 to 10.7 +/- 1.5 g/dL (p less than .001). The patients were grouped by their pretransfusion serum lactic acid values. In those patients with normal (less than 1.6 mmol/dL) serum lactic acid (n = 10), DO2 increased from 560 +/- 113 to 676 +/- 178 mL/min.m2 (p less than .02), and VO2 increased from 150 +/- 25 to 183 +/- 46 mL/min.m2 (p less than .02). However, in the increased serum lactic acid group (n = 17), VO2 was not significantly changed after transfusion (143 +/- 46 to 146 +/- 58 mL/min.m2) despite increased DO2 (515 +/- 163 to 609 +/- 251 mL/min.m2, p less than .01). CONCLUSIONS: Blood transfusion can be used to augment DO2 and VO2 in septic surgical patients. Increased serum lactic acid values do not predict patients who will respond. The absence of lactic acidosis should not be used in this patient population to justify withholding blood transfusions to improve flow-dependent VO2. Patients who have increased lactate concentrations may have a peripheral oxygen utilization defect that prevents improvement in VO2 with increasing DO2.
Prophylactic minitracheotomy in lung resections. A randomized controlled study. Thirty consecutive patients undergoing lung resections were randomized into two groups: Group A (n = 15) received minitracheotomy postoperatively and group B (n = 15) were control patients. Postoperative respiratory course was monitored by serial clinical assessments, chest x-ray examination, arterial blood gases, sputa bacterial cultures, and the patient's requirement and response to chest physiotherpy. The two groups were similarly matched in age (mean 58.5 years), smoking habits, pulmonary functions, and surgical procedures. Postoperative pulmonary complications of collapse/consolidation developed in 11 patients (two in group A and nine in group B) (p less than 0.03). Four patients (all in group B) required nimitracheotomy in addition to antibiotics and chest physiotherapy to treat their pneumonia. Chest physiotherapy requirement was less in group A than in group B, with a mean number of sessions of seven in group A and eight in group B and a mean total time of 92 minutes in group A and 112 minutes in group B. The mean duration of minitracheotomy was 4.13 days. Minor temporary symptoms resulted from the minitracheotomy in eight patients (42%) and included discomfort, voice changes, subcutaneous emphysema, and stridor. There was one case of long-term morbidity (5%)-skin scarring from wound infection at the site of the minitracheotomy. No postoperative deaths resulted. We conclude that the prophylactic use of minitracheotomy is safe and effective in decreasing postoperative respiratory complications in patients undergoing lung resections.
Prevalence of chronic migraine headaches--United States, 1980-1989. Migraine headaches, which are characterized by painful, disabling, and recurring symptoms, have no known cause, treatment, or cure. Quality population-based data are needed to improve epidemiologic understanding of chronic migraine headaches. This report uses data from the National Health Interview Survey (NHIS) to describe the prevalence of recent trends in the occurrence of chronic migraine headaches in the United States from 1980 through 1989.
Regulation of cerebral blood vessels by humoral and endothelium-dependent mechanisms. Update on humoral regulation of vascular tone. Recent studies suggest that humoral and endothelium-dependent mechanisms may play an important role in the cerebral circulation. Angiotensin may acutely and chronically increase resistance of large cerebral arteries and reduce cerebral microvascular pressure without changing cerebral blood flow. We hypothesize that the brain may sense reductions in microvascular pressure and initiate compensatory neurohumoral responses to raise arterial pressure. Vasopressin appears to play an important role in regulation of production of cerebrospinal fluid and brain fluid volume. Vasopressin also may be protective when intracranial pressure is elevated. Endothelium-dependent mechanisms also may have important influences on tone of cerebral vessels. Synthesis of the endothelium-derived relaxing factor nitric oxide, or a nitric oxide-containing compound, appears to influence both basal tone and responses of large cerebral arteries to acetylcholine in vivo. Large cerebral arteries dilate in response to increased blood flow in vivo, and this response may be mediated in part by release of a humoral factor by endothelium. Endothelium-dependent responses of cerebral arterioles to receptor- and nonreceptor-mediated agonists are impaired during chronic hypertension. The mechanism of impairment of endothelium-dependent responses of cerebral arterioles appears to involve production of an endothelium-derived contracting factor.
Hyperinsulinemia, sex, and risk of atherosclerotic cardiovascular disease BACKGROUND. The possibility that hyperinsulinemia may be involved in the etiology of atherosclerotic cardiovascular disease (CVD) was first suggested 20 years ago. During the last decade, this possibility has received support from three large prospective studies. METHODS AND RESULTS. In the present study, the association between CVD, glucose intolerance, obesity, and hypertension (the GOH conditions) and hyperinsulinemia was examined cross-sectionally in a representative sample (n = 1,263) of the adult Jewish population aged 40-70 years in Israel. Previously known diabetics were excluded. CVD comprising clinical or ECG evidence of ischemic heart disease, as well as clinical evidence of cerebrovascular or peripheral vascular disease, was identified in 97 men and 39 women. A significant (p less than 0.01) hyperinsulinemia-sex interaction was found for CVD rate, with the adjusted risk ratios (followed by 95% confidence limits), relative to the rate in 298 normoinsulinemic women, being 1.15 (0.68-1.95) in 328 normoinsulinemic men, 0.85 (0.48-1.49) in 277 hyperinsulinemic women, and 2.27 (1.33-3.08) in 360 hyperinsulinemic men. Age-adjusted CVD rates in men versus women were: a) similar and low among all normoinsulinemic normotensives and hyperinsulinemics free of any of the GOH conditions (all rates less than or equal to 6.5%); b) similar and high among normoinsulinemic hypertensives (13.4% versus 10.4%); c) significantly higher in men among hyperinsulinemic normotensives with glucose intolerance and/or obesity (15.2% versus 3.3%; p = 0.02) and all hyperinsulinemic hypertensives (21.5% versus 12.8%; p = 0.04). These trends remained significant after adjusting for age, ethnic group, and blood lipids. CONCLUSIONS. Therefore, hyperinsulinemia was associated with excess CVD risk in men but not in women, and all excess CVD risk in men was confined to hyperinsulinemic individuals in the presence of glucose intolerance, obesity, or hypertension.
Increased treatment of hypertension does not explain the decline in stroke mortality in the United States, 1970-1980. The steady decline in mortality from stroke in the United States accelerated markedly in the 1970s. It has been widely assumed that an increase in the rate of treatment of hypertension is the most likely explanation for this major public health achievement. An analysis of available information, however, suggests that improvements in the community control of hypertension in the United States in the period 1970-1980 have contributed in only a minor way. There were 45,357 fewer deaths from stroke in 1980 among those aged 35-74 years than might have been expected if the death rates had stayed the same as in 1970. Data from the National Health and Nutrition Surveys indicate that six million more people received antihypertensive medication in 1980 than in 1970. Results from a pooled analysis of randomized controlled trials of the treatment of hypertension suggest that between 6% and 16% of the reduction in stroke mortality was due to the increased treatment of hypertension. Epidemiological observations indicate that between 16% and 25% of the overall decline in stroke mortality can be attributed to the treatment of hypertension, suggesting that clinical trials probably underestimate the community-wide benefits of treatment. These results also suggest that at least three quarters of the decline in stroke mortality in the United States in the period 1970-1980 is due to factors other than antihypertensive treatment.
Possible roles of basic fibroblast growth factor in the pathogenesis of moyamoya disease: an immunohistochemical study. Prominent features of moyamoya disease are fibrocellular thickening of the intima and enhanced angiogenesis. The pathogenesis of moyamoya disease is, however, unknown. Basic fibroblast growth factor (FGF) is an angiogenic factor as well as a potent mitogen for a number of cell types including vascular endothelial and smooth-muscle cells. In order to test the possibility that basic FGF takes part in the pathogenesis of moyamoya disease, the authors tested for the presence of this factor using a mouse monoclonal antibody against human recombinant basic FGF. The surgical specimens studied included two sections of the superficial temporal artery (STA) and four samples of dura mater from four patients with moyamoya disease. Surgical specimens were obtained from three patients with other diseases as control tissue. Sections of the STA obtained from the patients with moyamoya disease showed strong basic FGF immunoreactivity in endothelial and smooth-muscle cells, while control sections had only faint and scattered immunoreactivity. All sections of the dura mater obtained from the patients with moyamoya disease also revealed more intense immunohistochemical staining of basic FGF in meningeal and vascular cells than did control sections. These observations indicate that the amount of basic FGF is increased in the tissues of patients with moyamoya disease; thus, basic FGF may play an important role in the pathogenesis of moyamoya disease.
Experimental non-steroidal anti-inflammatory drug-induced enteropathy in the rat: similarities to inflammatory bowel disease and effect of thromboxane synthetase inhibitors. We have validated an established animal model of acute inflammatory bowel disease in indomethacin-treated rats. Studies in both in vitro and in vivo 51chromium-labelled ethylenediamine tetra-acetate (51Cr-EDTA) permeability and tissue myeloperoxidase activity, a marker of inflammatory cell invasion, showed increased permeability and enzyme levels, respectively, in treated animals compared to controls (in vitro 51Cr-EDTA permeability: (mean (SE] control 0.10 (0.02) microliter/mg per tissue, experimental 0.17 (0.02) (p less than 0.01, 2 way analysis of variance); in vivo 51Cr-EDTA permeability: control 3.9 (1.3) (% dose recovered), experimental 12.1 (1.5) (p less than 0.01); tissue myeloperoxidase: control 10.8 (0.4) mU/mg, experimental 17.2 (0.5) p less than 0.01). Pretreatment or simultaneous treatment of indomethacin-treated animals with glucocorticoids, sulphasalazine, or tetracycline reduced the permeability changes and the tissue inflammatory response (in vitro 51Cr-EDTA permeability: (mean (SE] sulphasalazine + indomethacin 0.11 (0.2) microliter/mg tissue (p less than 0.01), prednisolone +/- indomethacin 0.12 (0.02) (p less than 0.01), tetracycline + indomethacin 0.12 (0.02) (p less than 0.01]. Glucocorticoids and sulphasalazine, but not tetracycline, administered after the indomethacin also partially corrected the permeability and inflammatory changes induced by indomethacin (in vitro 51Cr-EDTA permeability: sulphasalazine 0.15 (0.02) microliter/mg, p less than 0.02; prednisolone 0.12 (0.02) microliter/mg, p less than 0.01). This approach was used to investigate the effects of two different thromboxane synthetase inhibitors in indomethacin-treated animals. Simultaneous treatment with thromboxane synthetase inhibitors and indomethacin prevented the 51Cr-EDTA permeability and tissue myeloperoxidase increases induced by indomethacin alone (in vitro 51Cr-EDTA permeability: thromboxane synthetase inhibitors + indomethacin 0.11 (0.01) microliter/mg (p0.01); tissue myeloperoxidase: 11 (0.4) mU/mg, (p less than 0.01).
Risk factors for bilateral testicular germ cell tumors. Does heredity play a role? Twenty-three bilateral testicular germ cell tumors (four synchronous and 19 sequential tumors) were investigated for potential risk factors. The incidence of maldescensus testis was not found to be higher than in patients with unilateral disease. The histologic findings of the first tumor did not have any effect on the incidence of the second tumor. In 21 patients (four synchronous and 17 sequential tumors), histocompatibility antigens (HLA) were determined; HLA-B14 was increased significantly in the sequential tumor group. Tendencies toward an increase of HLA-DR5 and HLA-DR7 also were found. The HLA-DR1, HLA-DR3, and HLA-DR4 showed a tendency toward a decreased frequency. Therefore genetic factors might be important in the development of sequential bilateral testicular cancers.
Expression of platelet-derived growth factor and transforming growth factor and their correlation with cellular morphology in glial tumors. This study was undertaken to evaluate the role of two sets of growth factors, platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-beta), in the induction and maintenance of glial tumors and their phenotypic expression. Explants from eight malignant tumors, five benign tumors, and two nontumor glial cells were analyzed for levels of messenger ribonucleic acid (mRNA) expression of PDGFA, PDGFB, TGF-beta 1, and TGF-beta 2. Results were normalized to the mRNA expression of tubulin, a "housekeeping" gene present in glial cells. Of the 15 explants tested, PDGFB was seen in six, all of which were malignant tumors; PDGFA was seen in all 15 with much higher levels expressed in malignant tumors; and TGF-beta 1 and TGF-beta 2 were seen in all 15 without a clear difference between cell types, although expression tended to be higher in malignant tumors. This project supports the theory that the induction and maintenance of glial tumors is likely to be a multifactorial phenomenon.
The risk of ligation of the left renal vein in resection of the abdominal aortic aneurysm. The left renal vein can be ligated during aortic operation to attain better access to the perirenal aorta. This maneuver has been considered safe, with a low incidence of postoperative renal complications. This study was done to evaluate the risk of left renal vein ligation and its influence on renal function in patients with elective resection of abdominal aortic aneurysms. The records of 332 patients undergoing elective repair of abdominal aortic aneurysms during a five year period were reviewed. The clinical and operative data of patients who had left renal vein ligation and those who did not were similar. Left renal vein ligation was not associated with an increased mortality rate but was strongly associated with an increase in serum creatinine level and a clinical diagnosis of postoperative azotemia. Nine of 13 patients who had left renal vein ligation had postoperative azotemia compared with 21 of 319 patients without left renal vein ligation (p less than 0.001). The mean change of preoperative and postoperative creatinine value was an increase of 1.92 milligrams per deciliter in patients with left renal vein ligation in contrast with 0.26 milligram per deciliter in patients without ligation (p less than 0.00075). Thus, ligation of the left renal vein increases the risk of postoperative renal complications and its use should be selective.
Choriocarcinoma of the septum pellucidum: case report. A case of choriocarcinoma of the septum pellucidum is presented. The patient, a 6-year-old boy, demonstrated high levels of human chorionic gonadotropin in his urine, serum, and cerebrospinal fluid, and precocious puberty. The physical conditions and laboratory data returned to normal after surgical removal of the tumor, whole brain irradiation, and chemotherapy. Currently, there is no evidence of recurrence at 5 months after surgery.
The combined antiischemic effects of the thromboxane receptor antagonist SQ 30,741 and tissue-type plasminogen activator. The thromboxane-receptor antagonist, SQ 30,741, may be used as adjuvant therapy for thrombolysis and has also been shown to have antiischemic activity that is independent of its thrombolytic activity. Since tissue-type plasminogen activator (t-PA) and SQ 30,741 may be administered simultaneously, we determined whether the antiischemic effects of SQ 30,741 can be potentiated by t-PA. This was accomplished by combining doses of t-PA and SQ 30,741, which alone were not cardioprotective. Anesthetized dogs were subjected to left circumflex coronary artery occlusion for 90 minutes and reperfusion for 5 hours. The dogs were treated during reperfusion with a dose of t-PA that caused approximately a 30% reduction in plasma fibrinogen alone or in combination with 1.5 mg/kg + 0.4 mg/kg/hr SQ 30,741, which started 10 minutes after initiation of ischemia. At these doses, neither t-PA nor SQ 30,741 alone significantly reduced infarct size (57% +/- 6%, 50% +/- 10%, 57% +/- 6% of the left ventricular area at risk for vehicle controls, t-PA, and SQ 30,741 respectively); however, combination treatment resulted in a significant reduction in infarct size (37% +/- 5% of the left ventricular area at risk). Higher doses of t-PA and SQ 30,741 alone significantly reduced infarct size. The protective effects of t-PA and SQ 30,741 occurred without altering peripheral hemodynamic status. No differences in collateral or reperfusion blood flow were observed between groups. Thus although SQ 30,741 may act to improve the efficacy of thrombolysis, t-PA may in turn enhance the antiischemic activity of SQ 30,741 or at least reduce the threshold dose.
Measurement of tissue oxygen tension: comparison between two subcutaneous oxygen tonometers. We compared the 95% response time (95% RT) of two tissue oxygen tonometers under two sets of circumstances. We first evaluated the devices during normoxia, hyperoxia, and anoxia in vitro, using a transcutaneous PO2 electrode (PtcO2) as the reference. The responses to normoxia and to different grades of hyperoxia were examined in vivo in 8 healthy volunteers to assess the relationship between changes in subcutaneous PO2 and PtcO2, an estimate of arterial PO2 (PaO2). One subcutaneous method (ScA) used a technique based on a polarographic needle electrode in situ connected to an ammeter; the second method (ScB) was based on a blood gas analyzer system first described by Hunt (Lancet 164;2:1370). ScA and PtcO2 both responded to stepwise changes in ambient oxygen concentration (21-100%) in vitro within 10 seconds; the 95% RT of ScA was 1.39 +/- 0.5 to 2.39 +/- 0.8 minutes and that of PtcO2 was 0.32 +/- 0.1 to 0.49 +/- 0.1 minutes. ScB had a lag of 3 minutes, and the 95% RT was 6.75 +/- 0.5 to 8.2 +/- 0.8 minutes. In contrast to the results in vitro, the response of ScA to changes in FiO2 in vivo was delayed compared with the rapid response of PtcO2, reflecting the physiologic delay of tissue PO2 in response to increased PaO2. The time lag and the long 95% RT of ScB were even more evident in vivo. ScA reacted three to four times faster than ScB, both in vitro and in vivo, to changes in the oxygen environment. The in vitro 95% RT of ScA to changes in ambient oxygen varied from 2 to 3.5 minutes.