123rc/medical_text huggingface dataset:
Primary neoplasms of the central nervous system in children. Modern diagnostic imaging techniques are able to detect primary neoplasms of the central nervous system (CNS) in children safely and accurately but with less specificity as to cell type or degree of malignancy. These neoplasms, often peculiar in cell type and size, mediated by hydrocephalus in their clinical presentation, demand careful and often extensive imaging techniques best to evaluate their geography and character. Added to these basic observations, determination of the neoplasm from surrounding edema, detection of possible spread, and evaluation of residual or recurrent neoplasm are prime responsibilities of the pediatric neuroradiologist toward the child, neurosurgeon, and oncologist.
Antecedent medical diseases in patients with amyotrophic lateral sclerosis. A population-based case-controlled study in Rochester, Minn, 1925 through 1987. Odds ratios (ORs) were estimated for the prevalence of antecedent endocrine, metabolic, or vascular diseases among 45 patients with amyotrophic lateral sclerosis from the Rochester, Minn, population compared with 90 control subjects matched for sex, year of birth, period of observation, and residence. Hypertension occurred less frequently in male patients with amyotrophic lateral sclerosis (4%) than in control subjects (30%; OR = .10). Because of small population size, no conclusions can be drawn with respect to the following antecedent conditions: thyroid disease (OR = 1.61), coronary artery disease (OR = .58), obesity (OR = .52), diabetes (OR = 1.00), cerebrovascular disease (OR = .21), and peripheral vascular disease (OR = 1.23). The heterogeneity of antecedent thyroid disease makes it highly unlikely that any specific thyroid lesion is causally associated with most cases of amyotrophic lateral sclerosis. Hypertension may be a marker for protective factors against the development of amyotrophic lateral sclerosis in men.
Fungal meningitis. Fungal meningitis tends to be a subacute or chronic process; however, it may be just as lethal as bacterial meningitis if untreated. There are many similarities between the pathogenic fungi. Most of the fungi are aerosolized and inhaled, and initiate a primary pulmonary infection which is usually self-limited. Hematogenous dissemination may follow the initial infection, with subsequent involvement of the CNS. Rarely, trauma or local extension provides the route to CNS infection. The host is frequently, although not always, immunosuppressed. The hyphae of molds generally cause focal disease with hemorrhagic necrosis secondary to vascular thrombosis. The yeasts tend to cause a more diffuse process with the base of the brain being primarily affected, such that hydrocephalus is seen as a frequent complication of chronic disease. Diagnosis may be difficult, as the CSF may be normal, with negative smears and sterile cultures, although more often there is at least one abnormality indicating disease. Serologies (if available, depending on the fungus) may point towards the proper diagnosis, as may a careful travel history. Currently, amphotericin B is still the drug of choice in most situations; however, the newer azole antifungal agents offer great promise, especially in the treatment of cryptococcal meningitis. The precise role of such agents will remain unclear until appropriate large-scale studies of their effectiveness have been completed. The treatment of the unusual CNS mycoses will continue to be based on clinical experience, and reports of the use of new azoles in these diseases need to be critically evaluated.
Pharmacologic treatment of noncognitive behavioral disturbances in elderly demented patients. Fifty-nine elderly residents of long-term care facilities who had DSM-III diagnoses of dementia were studied in an 8-week randomized, double-blind comparison trial of haloperidol, oxazepam, and diphenhydramine to test the efficacy of these agents in the treatment of clinically significant behavioral disturbances in patients with dementia. All three agents demonstrated modest but significant efficacy as measured by clinician ratings of agitated behavior and activities of daily living. The absolute magnitude of improvement was greater for haloperidol and diphenhydramine than for oxazepam, but differences among groups did not approach statistical significance. Frequencies of acute adverse events during the trial were similar across the drug treatment groups. Although these drugs may differ in terms of long-term safety and efficacy, they appear to be equivalent for short-term management of agitated behavior in severely demented patients.
Myoglobin depletes renal adenine nucleotide pools in the presence and absence of shock. To assess whether myoglobin adversely affects renal adenylate pools, rats were infused with purified myoglobin (50 mg/100 g body wt) for two hours and renal ATP, ADP, and AMP levels were measured in the absence of shock, after 25 minutes of hemorrhagic shock (55 to 60 mm Hg) or 30 minutes post-recovery. In the absence of shock, myoglobin lowered ATP by 24% (assessed 65 min post-infusion) without affecting renal blood flow (RBF). This effect was completely blocked by deferoxamine (DFO) treatment and it could not be reproduced by ribonuclease infusion (a non-Fe containing, but filtered, protein). Myoglobin + shock caused a three- to fourfold greater decline in ATP than did shock alone despite comparable RBFs. Shock plus myoglobin, but neither one alone, induced substantial S1/S2 proximal tubular morphologic damage and a severe reduction in creatinine clearance, confirming synergistic injury. Ribonuclease completely reproduced myoglobin's effect on shock-induced adenylate profiles. DFO +/- hydroxyl radical scavenger therapy (Na benzoate) did not block the myoglobin shock effect on adenylate pools. Post-shock adenylate recovery was not compromised by myoglobin pre-treatment. If renal artery occlusion (RAO), rather than shock, was used as the ischemic challenge, myoglobin had no discernible impact on adenine nucleotide content. This study concludes that: 1) myoglobin modestly lowers baseline adenylate pools due to an Fe dependent mechanism; 2) myoglobin drastically accentuates shock-induced adenylate depletion by a non-hemodynamic/non-Fe dependent mechanism; 3) myoglobin nephrotoxicity cannot be attributed solely to tissue iron loading; and 4) the RAO model can completely mask important influences on ischemic cellular energetics.
Pathophysiology of hypertension in blacks. The pathophysiology of hypertension in the black population differs to some extent from that of the nonblack population. Although black hypertensives exhibit enhanced sodium retention, expanded plasma volume, lower plasma renin activity, and a greater increase in blood pressure in response to high levels of Na+ intake compared with nonblack hypertensives, there is considerable heterogeneity in these studies. Alterations in ion transport mechanisms, such as a decrease in Na+K(+)-ATPase activity and Na+K+ cotransport, have been demonstrated in the black hypertensive population. Those features provide the physiologic basis for the differential response to monotherapy with diuretics and, perhaps, with calcium channel blockers, that is observed in black hypertensives, particularly when compared with responses to beta-blockers or angiotensin converting enzyme inhibitors.
Spontaneous neurodegeneration in transgenic mice with mutant prion protein Transgenic mice were created to assess genetic linkage between Gerstmann-Straussler-Scheinker syndrome and a leucine substitution at codon 102 of the human prion protein gene. Spontaneous neurologic disease with spongiform degeneration and gliosis similar to that in mouse scrapie developed at a mean age of 166 days in 35 mice expressing mouse prion protein with the leucine substitution. Thus, many of the clinical and pathological features of Gerstmann-Straussler-Scheinker syndrome are reproduced in transgenic mice containing a prion protein with a single amino acid substitution, illustrating that a neurodegenerative process similar to a human disease can be genetically modeled in animals.
Benign cystic teratoma manifested as an umbilical hernia. We have reported a case of dermoid tumor manifested as an umbilical hernia. Resection led to complete recovery.
The agent of bacillary angiomatosis. An approach to the identification of uncultured pathogens BACKGROUND. Bacillary angiomatosis is an infectious disease causing proliferation of small blood vessels in the skin and visceral organs of patients with human immunodeficiency virus infection and other immunocompromised hosts. The agent is often visualized in tissue sections of lesions with Warthin-Starry staining, but the bacillus has not been successfully cultured or identified. This bacillus may also cause cat scratch disease. METHODS. In attempting to identify this organism, we used the polymerase chain reaction. We used oligonucleotide primers complementary to the 16S ribosomal RNA genes of eubacteria to amplify 16S ribosomal gene fragments directly from tissue samples of bacillary angiomatosis. The DNA sequence of these fragments was determined and analyzed for phylogenetic relatedness to other known organisms. Normal tissues were studied in parallel. RESULTS. Tissue from three unrelated patients with bacillary angiomatosis yielded a unique 16S gene sequence. A sequence obtained from a fourth patient with bacillary angiomatosis differed from the sequence found in the other three patients at only 4 of 241 base positions. No related 16S gene fragment was detected in the normal tissues. These 16S sequences associated with bacillary angiomatosis belong to a previously uncharacterized microorganism, most closely related to Rochalimaea quintana. CONCLUSIONS. The cause of bacillary angiomatosis is a previously uncharacterized rickettsia-like organism, closely related to R. quintana. This method for the identification of an uncultured pathogen may be applicable to other infectious diseases of unknown cause.
Effect of marked peripheral leukocytosis on the leukocyte count in ascites. Patients with high peripheral leukocyte counts are sometimes found to have high leukocyte counts in ascitic fluid in the presence of negative cultures. To determine if peripheral leukocytosis (greater than or equal to 20 x 10(9)/L) by itself can result in high leukocyte or neutrophil counts in ascites, 29 patients were studied. A total of 31 paracenteses were performed in these patients as soon as the high peripheral leukocyte count was determined. Culture of ascitic fluid was performed using blood-culture bottles. The mean peripheral leukocyte count was 29.3 +/- 9.3 x 10(9)/L, with a mean neutrophil count of 19.9 +/- 6.5 x 10(9)/L. The mean ascitic fluid neutrophil count was 0.064 +/- 0.054 x 10(9)/L (range, 0.007 to 0.197 x 10(9)/L). No significant correlation was found between peripheral neutrophil (or leukocyte) count and neutrophil (or leukocyte) count in ascitic fluid. Marked peripheral leukocytosis (or neutrophilia) does not seem to have an effect on the leukocyte or neutrophil count in ascitic fluid.
Three staged approach to the surgical management of renal cell carcinoma extending into the right atrium. Case report. Left renal cell carcinoma extending into the right atrium was treated by angioinfarction, removal of right atrial tumour using cardiopulmonary bypass and ten days later abdominal radical nephrectomy and inferior vena cava thrombectomy. Twenty four months later the patient remains well with no evidence of tumour recurrence.
Salt and hypertension--future directions. The comments that follow reflect the personal views of this author regarding some useful directions of research in the field of salt and hypertension. From a physiological perspective, salt sensitivity is defined, and the merits and limitations of certain animal models of hypertension used to study this issue are discussed. The need to more clearly define the mechanisms that detect sodium intake and control the renal excretion of sodium is discussed. Additionally, the need to better understand the relation between sodium homeostasis, volume regulation, and the consequences of dysfunction in these regulatory system on the arterial vasculature and interstitial matrix is emphasized. The necessity for the application of new tools and approaches in a number of investigative areas is discussed. Finally, the necessity of equally imaginative whole animal and cell/molecular research and efforts to merge and integrate the data obtained at the cellular level with that of intact systems is emphasized.
Malignant fibrous histiocytoma of the conjunctiva. Malignant fibrous histiocytoma (MFH) of the conjunctiva is an extremely rare tumour, and only three previous cases have been reported. We describe two patients with MFH of the conjunctiva: a 58-year-old white male with epibulbar tumour who had exenteration and is alive after five years' follow-up, and a 3 1/2-year-old African girl with xeroderma pigmentosum and an MFH of her right eye conjunctiva, the first reported case of this association. The characteristics and the methods of diagnosis of MFH are discussed.
Renal vein renins: inability to predict response to revascularization in patients with hypertension. To determine whether the captopril-stimulated renal vein renin ratio (CSRVRR) could enable identification of patients with hemodynamically significant renovascular lesions who would respond to revascularization, the authors measured CSRVRRs in 143 consecutive patients with hypertension who had been selected because of clinical features suggestive of renovascular hypertension. All patients underwent conventional renal arteriography. Renovascular hypertension was the final diagnosis if revascularization resulted in cure or improvement in blood pressure. Complete data were available for 133 patients. Twenty patients had renovascular hypertension; CSRVRR was greater than 1.5 in 13 of these 20 patients (sensitivity, 65%). However, it was also greater than 1.5 in 54 of the 113 patients without renovascular hypertension (false-positive rate, 47.8%). The positive predictive value of CSRVRR was 18.6%; the negative predictive value, 89.3%. It is concluded that CSRVRR is not sufficiently sensitive to enable prediction of which patients will respond to revascularization and is not specific enough to exclude patients who do not have renovascular hypertension.
Daytime hypertension in obstructive sleep apnea. Prevalence and contributing risk factors. We examined the prevalence of daytime hypertension in a modern sample of patients with obstructive sleep apnea (OSA) and assessed the relative risk factors contributing to the development of hypertension in this disorder. Daytime hypertension was present in 92 (45 percent) of 206 male and female patients with OSA. Stepwise logistic regression revealed that only age and body mass index (BMI) were predictors of hypertension in this population. A subsample of 152 male patients with OSA was then compared to 904 men identified from a geographically and ethnically similar general population. When one controlled for age and BMI, the prevalence of hypertension in the two groups was the same except for those aged 25 to 44 years who were markedly obese (BMI greater than 31 kg/m2). In this group, 47 percent of the patients with OSA were hypertensive vs 26 percent of control subjects (p less than 0.05). Our data suggest that the high prevalence of hypertension in OSA is primarily related to age and the excess obesity seen in these patients. In morbidly obese young patients with OSA, factors directly related to OSA may also be contributing to the development of hypertension. With increasing age, other competitive risks may obscure any independent effect that OSA may exert.
Prevention of a false diagnosis of sexually acquired reactive arthritis by synovial lymphocyte responses. Three cases are reported in which a diagnosis of sexually acquired reactive arthritis might have been made erroneously from the history, but the enteric origin of the reactive arthritis was evident from synovial lymphocyte responses. The importance of making the correct diagnosis and the avoidance of unwarranted spousal dysharmony is stressed.
Prospective study on prevalence of esophageal chest pain in patients referred on an elective basis to a cardiac unit for suspected myocardial ischemia. The prevalence of esophageal chest pain was studied prospectively in patients referred on an elective basis to a cardiac unit for suspected myocardial ischemia. A group of 248 consecutive patients without previously documented heart disease was admitted for elective diagnostic coronary angiography. The clinical history classified 185 patients as having anginal pain and the coronary angiogram was normal in 48 of them. In 37 of these 48 patients full esophageal testing was performed including 24-hr intraesophageal pH and pressure recordings with indication of chest pain episodes as well as a number of esophageal provocation tests, ie, acid perfusion, edrophonium stimulation, balloon distension, and ergonovine stimulation, all performed under continuous esophageal manometric and electrocardiographic monitoring. In 19 of these 37 patients, the familiar chest pain could be reproduced by esophageal provocative testing without ischemic ST-T segment alterations; six of these 19 patients had also a positive 24-hr pH and pressure recording. These data strongly suggest an esophageal origin of chest pain in half the patients with typical angina and a normal coronary angiogram.
Bronchial anomaly of the right upper lobe. This case report presents a rare anomaly of right upper lobe bronchial anatomy. During routine right upper lobe resection for carcinoma, a common right upper and middle lobe bronchus was found. The resection was completed as a right upper and middle bilobectomy. Knowledge of this uncommon variant was beneficial in performing the pulmonary resection. A review of the literature is presented.
Limb reconstruction with vascularized fibular grafts after bone tumor resection. Limb-salvage operations are being used with increasing frequency for patients with malignant bone tumors. For children, when a biologic reconstruction is desired, the choice is often between conventional and vascularized fibular grafts. An experimental study was performed in dogs to compare the two types of fibular grafts for bridging segmental defects in the radius and ulna. Twenty-six adult dogs were divided into two groups and studied at intervals of two, three, four, six, and 12 months after transplantation. The conventional grafts healed by creeping substitution i.e., they were first partially resorbed before new bone was laid down. In contrast, the vascularized fibulae maintained their normal structure and hypertrophied by subperiosteal new bone formation. The conventional fibulae eventually hypertrophied but much later than the vascularized grafts. The vascularized grafts were stronger at four and six months. Between six and 12 months, both grafts remodeled to resemble the size and shape of the forearm bones they were replacing. These experimental results have influenced the treatment of patients. Vascularized fibular grafts are ideal for diaphyseal defects greater than 10 cm long, especially in very young children, a poorly vascularized bed, or when bone healing is delayed by chemotherapeutic agents. To maximize hypertrophy, an external fixator is used to immobilize the graft rather than a plate, which acts as a stress shield.
The pathophysiology of anoxic injury in central nervous system white matter. White matter of the mammalian brain is susceptible to anoxic injury, but little is known about the pathophysiology of this process. We studied the mechanisms of anoxic injury in white matter using the isolated rat optic nerve, a typical central nervous system white-matter tract. Optic nerve function, measured as the area under the compound action potential, rapidly failed when exposed to anoxia. Postanoxic recovery was variable, depending on duration of the anoxic insult; after a standard 60-minute period of anoxia, the compound action potential recovered to 28.5% of control. Irreversible anoxic injury was critically dependent on extracellular Ca2+; maintaining the tissue in zero [Ca2+] solution throughout the anoxic period resulted in 100% compound action potential recovery. Increasing perfusate [Ca2+] during anoxia from zero to 4 mM resulted in progressively less recovery. Anoxic damage to the optic nerve appears to depend on the gradual accumulation (over tens of minutes) of Ca2+ in a cytoplasmic compartment. The inorganic Ca2+ channel blockers Mn2+ (1 mM), Co2+ (1 mM), or La3+ (0.1 mM) had no effect on recovery of the compound action potential after anoxia; only Mg2+ (10 mM) significantly improved recovery. Treatment with the dihydropyridine Ca2+ channel blockers nifedipine (1-10 microM) or nimodipine (1-40 microM) also had no effect on recovery from anoxia. Thus, Ca2+ influx during anoxia does not occur via conventional Ca2+ channels. Preliminary evidence suggests that this Ca2+ influx may occur via other cation channels that are imperfectly selective for Ca2+ or via the Na(+)-Ca2+ exchanger.
Fibrosing mediastinitis with coronary artery involvement. This case report describes a patient with chronic fibrosing mediastinitis involving the entire intrapericardial aorta, innominate artery, and the base of the heart with involvement of the proximal segments of the coronary arteries. This finding was unsuspected before emergency coronary artery bypass grafting. Coronary stenosis due to fibrosing mediastinitis is a rare complication of fibrosing mediastinitis. Owing to the extensive fibrosis, the normal bypass, cardiac preservation, and revascularization techniques required alteration and are discussed.
Inflammatory pseudotumor of the liver. Inflammatory pseudotumor of the liver is an extremely rare entity. Because of its unusual clinical presentation and confusing histologic picture, a diagnosis of malignancy is frequently made. Thus the surgeon is closely involved with the case and extensive procedures are not uncommon. However, this lesion is benign and will even regress spontaneously, making radical surgical procedures contraindicated. The difficulty lies in establishing an accurate diagnosis and the histologic pitfalls of this particular process. Conservative therapy can then be applied, avoiding surgical morbidity.
A phase I trial of cisplatin in hypertonic saline and escalating doses of 5-fluorouracil by continuous intravenous infusion in patients with advanced malignancies. Thirty-four patients with incurable solid tumors were treated in a Phase I trial with a fixed dose of high-dose cisplatin (CDDP) administered in hypertonic saline and escalating doses of infusional 5-fluorouracil (5-FU). Five treatment levels of 5-FU, ranging from 500 to 900 mg/m2/day for 5 days, were studied. Leukopenia, thrombocytopenia, and oral mucositis were the dose-limiting toxicities encountered. Nephrotoxicity was minimal. Ototoxicity and peripheral neuropathies were rare and mild in this patient group, but most patients received only a small number of treatment cycles. Diarrhea was not dose-limiting. Two complete responses (one non-small cell lung cancer and one sweat gland carcinoma) were observed. No other major responses were noted. With the dose of CDDP set at 35 mg/m2/day for 5 consecutive days, the maximum tolerated dose (MTD) of a concurrent 5-day 5-FU infusion was found to be 900 mg/m2/day. The recommended dosages for Phase II trials are 35 mg/m2/day CDDP and 800 mg/m2/day 5-FU for 5 consecutive days. Cancers of the lung, breast, gastrointestinal tract, and genitourinary tract would be reasonable targets for Phase II studies.