Visceral calcification in patients with AIDS may not always be due to Pneumocystis carinii.
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Biomedical subjects
Publications and source records attributed to A Kolin.
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Left ventricular systolic and diastolic function before, during, and after a 2-hour intravenous infusion of epinephrine at either 0.5 micrograms/kg/min or 2 micrograms/kg/min were assessed by pressure-volume data obtained by conductance catheter micromanometer technique and correlated with cardiac ultrastructure and plasma levels of epinephrine in neonatal (3-5 days old, n = 12) versus adult (3-4 months old, n = 11) pigs. Administration of epinephrine at 0.5 micrograms/kg/min resulted in an increase in end-systolic elastance (Ees) only in adults, whereas at 2.0 micrograms/kg/min Ees increased in both groups. After 2-hour administration of epinephrine at 2.0 micrograms/kg/min, Ees decreased significantly (p less than 0.05) from the preinfusion baseline value of 8.9 +/- 2 (mean +/- SD) to 5 +/- 1.7 mm Hg/ml, and a significant (p less than 0.05) increase in left ventricular volume elasticity (VdP/dV) from 0.4 +/- 0.02 to 1.4 +/- 0.2 mm Hg occurred in neonates versus no change from baseline in either Ees or VdP/dV in the adults. These changes in the neonates were associated with sarcolemmal rupture and mitochondrial Ca2+ granule deposition versus normal cardiac ultrastructure in the adults. We conclude that the neonatal myocardium is more susceptible to cardiotoxicity from circulating epinephrine.
A granulomatous response to neoplastic structures was found in three cases of resected small-cell anaplastic carcinoma of the lung. This consisted of almost continuous rims of palisading epithelioid cells surrounding viable, necrotizing, and necrotic tumor nests. None of the patients had received chemotherapy or radiation treatment prior to surgery, and no clinical, microbiological, or histological evidence of tuberculosis, fungal infection, or rheumatoid disease was found. The granulomatous rim seems to be a response to spontaneous tumor decay.
The protective effects of beta 1-adrenergic blockade with metoprolol (Betaloc Astra) were demonstrated in the gerbil model of myocardial injury provoked by acute ischaemic brain lesions. The myocardial injury was reversible and lipid droplet accumulation was its most striking morphological feature. These droplets were easy to measure in EM photographs and their size was expressed as percentage of sarcoplasmic volume. The EM data of fat accumulation were compared in hearts of carotid-ligated animals with and without metoprolol pretreatment, and in animals with the carotid isolated only, at standard intervals 3-48 h after operation. While in carotid-ligated-only animals the average myocardial fat contents rose to a peak of 1.9% at 10 h, in metoprolol pretreated animals the amount of fat was always significantly lower and started to return earlier to basal values (peak at 6 h, 1.1%). In carotid-isolated-only animals, fat accumulation peaked at 6-10 h (1.1%) and returned quickly to normal levels (0.34 +/- 0.18%). This effective pharmacological blockade with metoprolol strongly supports the concept of catecholamine mediation between acute intracranial lesions and myocardial injury. The background and significance of myocardial fat accumulation is discussed. The EM morphometry of fat droplets appears to be a suitable tool for quantification of reversible myocardial damage most useful for experimental evaluation of cardioprotective measures. As changes in succinic dehydrogenase histochemistry (from 'myofibrillar' to 'granular' pattern) correlated with EM measured fat accumulation, the simplicity and speed of the SDH method recommends itself for fast orientation about presence of myocardial damage.
In the present investigation an attempt was made to ascertain whether nonviral liver impairment in rats affects the THelper/TSuppressor ratio. Two hepatotoxic agents were used: (i) galactosamine (GA), which causes a drug-induced hepatitis-like damage, and (ii) orotic acid (OA), which induces fatty changes. Since these two substances act as antidotes to one another they were administered to rats either separately or simultaneously. GA caused severe liver damage documented by a 104-, 48-, and 1.6- fold rise in the plasma concentrations of ALT, AST, and ALP and by multiple foci of hepatocyte necrosis. This was followed by a drop in TH/TS ratio from 2.25 observed in the controls to 0.89 in the GA-treated rats. All of these phenomena were prevented by concurrent administration of GA and OA. OA alone did not show an effect on the liver with respect to changes in plasma enzyme concentrations and by light microscopic analysis. However, OA caused a drop in the TH/TS ratio from 2.25 to 1.55. Neither GA nor OA produced a change in TH/TS ratios in in vitro experiments.
The pathogenesis of scars in lung carcinomas was studied in 57 consecutively resected small (less than or equal to 3 cm) peripheral lung cancers. Central, pigmented scars rich in elastic fibers were most frequently found in adenocarcinomas with predominantly non-destructive, intraalveolar growth pattern. In these cancers with elastin-rich scars, active neoplastic occlusion of one or more arteries was almost always found (96%). Infarction of tumor tissue and its supporting pulmonary stroma was frequently seen separating the central scar from the viable peripheral tumor zone. The elastic fibers of alveolar walls survived and condensed into a compact central scar. Based on these observations, it is suggested that scarring in peripheral lung cancers is often caused by mechanisms unique to the lung. Lung cancers often invade and occlude branches of pulmonary arteries, causing ischaemic necrosis (infarction) of the neoplasm and its stroma. In these neoplasms, often growing mainly in air spaces and preserving the pulmonary framework as their stroma, the elastic fibers of the aLveoli remain preserved despite necrosis, so that the alveolar elastic collapses to form the characteristic elastin-rich scar following absorption of necrotic debris.
Acute cerebral infarction in gerbils, produced by unilateral carotid ligation, was used as a model to investigate secondary myocardial changes. The extent of the myocardial damage revealed by succinic dehydrogenase (SDH) histochemistry and by release of myocardial creatine phosphokinase (MB-CK) was measured in gerbils sacrificed from 3 to 48 h after either carotid ligation, carotid isolation only or skin incision only. For technical reasons dead animals were excluded from analysis. Of surviving ligated animals 74% developed neurological deficits related to brain ischaemia. A significant weight increase in the ipsilateral hemisphere was found at 6-10 h, and maximal histological damage at 16 h, both partially reversible thereafter. Non-ligated animals did not develop neurological changes, and showed neither brain swelling nor cerebral histopathology. Extensive cardiac damage was shown by the SDH method from 3 h postoperatively, and confirmed by the elevated serum levels of MB-CK in the carotid-ligated group. The SDH changes were identical with those described in the hearts of patients with acute intracranial lesions, and appeared to be reversible. The effect of beta-adrenergic blockade was assessed in this model. Metoprolol tartrate injected intraperitoneally 3 h before and 1 h after carotid ligation (10 mg/kg each dose) significantly decreased the extent of myocardial damage as estimated both with SDH histochemistry and MB-CK serum levels. It had no effect on the ischaemic brain changes. These results strongly support the concept of catecholamine mediation of myocardial injury resulting from acute brain lesions.
In a retrospective study using histologic material from resected pulmonary (n = 113), renal (n = 26), and bowel (n = 26) carcinomas, the frequency of neoplastic invasion of arteries was investigated. In contrast to 3.8 per cent for both renal and bowel carcinomas, at least 58 per cent and probably as many as 87 per cent of lung cancers invaded pulmonary artery branches. Arterial invasion was followed by thrombosis, organization by granulation tissue, and scarring. No correlation was found between neoplastic invasion of arteries and histologic type and grade of tumors or lymph node status at time of operation. The elastic laminae of arterial walls are apparently not a sufficiently strong barrier against neoplastic growth. The resistance of systemic arteries most likely depends on the higher blood pressure in their lumina, which results in a steep pressure gradient through their walls that successfully opposes the cancer advance. The lower pulmonary artery pressure appears to be insufficient to prevent this tumor cell progress.
Severe, atypical osteoarthritis of the metacarpophalangeal and elbow joints in a jackhammer operator is reported. Articular tissue resected at surgery demonstrated gross fibrillation and histologic evidence of calcification of articular cartilage, and multiple, bony fragments embedded in the synovium. Operation of a pneumatic drill may accentuate a tendency toward development of osteoarthritis in workers who are predisposed to the disease and may also cause it to localize at unusual sites such as the elbow, shoulder, wrist, and metacarpophalangeal joints.
While using the natural killer (NK) cell-associated HNK-1 antibody in a panel of hematopoietic cell markers, the authors found that metastatic tumor cells in the bone marrow of a patient with disseminated prostatic carcinoma stained strongly with this antibody using an indirect immunofluorescence technique. More than 50% of cells from the patient's prostate also reacted with HNK-1. Subsequent study of frozen sections of prostate tissue from patients with benign prostatic hypertrophy (BPH) showed that HNK-1 reacted with prostatic epithelium and the contents of the glandular lumina. Two other markers associated with NK cells (OKM1 and OKT3) were not detected on nonneoplastic or neoplastic prostatic epithelial cells using a two-color immunofluorescence technique. Recent reports have shown that the HNK-1 antibody also detects an antigen on cells of neuroectodermal origin. The authors have concluded that HNK-1 also reacts with prognostic epithelium in patients with BPH and may be useful as another marker for metastatic carcinoma of the prostate.
Recurrent acute otitis media (RAOM) is a distressing clinical manifestation of middle ear pathology, mainly expressed in the first two years of life. In this controlled study, prophylactic treatment by phenoxymethyl penicillin reduced significantly the frequency of RAOM in 60 children, as compared to 48 children who received a short ampicillin course only on the occasion of an acute otitis media episode. The importance of breastfeeding, age at initial episode, the type of treatment given and the pertinent literature is discussed. A working hypothesis of this prophylactic treatment is suggested.
Two cases of lymphomatoid granulomatosis affecting the gastrointestinal tract in the form of gastric ulceration and intestinal perforation are described. This rare presentation of lymphomatoid granulomatosis is discussed in the context of previous reviews of the disease, and it is suggested that clinically overt gastrointestinal involvement represents a very poor prognostic indicator in this condition.
The morphological aspect of the antineoplastic defence mechanism was studied in Sewall-Wright strain 13 guinea pigs using isogeneic line 2 hepatoma cells. When these tumour cells were injected i.p. into isogeneic hosts, they grew rapidly and always killed their hosts within 8 weeks. An intradermal injection of line 2 hepatoma cells in strain 13 guinea-pigs 3 weeks before i.p. challenge with the same tumour cells protected such pre-immunized animals. While the intradermal inoculum failed to grow, it conferred sufficient immunity to enable the host to reject the tumour after a short period of growth. This phenomenon showed immunological specificity since intradermal injection of allogeneic hepatoma cells did not offer this protection. By using sequential histological analysis in these preimmunized animals, we were able to identify 2 sets of cells migrating into and around tumour modules in relation to tumour cell death. Firstly, small numbers of small lymphocytes were observed at the earliest signs of tumour cell damage. They were most likely the effectors of antineoplastic defence mechanisms. Secondly, a variety of numerous inflammatory cells including macrophages were observed later when the tumour was necrotic, and these cells were considered to be present as a response to tumour cell death.
Thirty-five patients with perennial rhinitis were treated with beclomethasone dipropionate nasal aerosol three times daily for 48 weeks. There was no evidence at the end of the study of any adverse effects from the topical steroid as assessed by biopsy studies of the nasal mucus membrane and by negative nasal cultures for C. albicans.
We have studied the effects of preimmunization with a conjugate of beta-subunit of choriogonadotropin and tetanus toxoid (CG beta-tt) on the growth of the implanted R 3230 AC mammary adenocarcinoma (in Fischer 344 rats) and the implanted 5123 1-1 hepatoma (in Buffalo rats) after 20 days, in order to determine if the in vivo production of antibodies against CG could modify the relationship between host and malignant growth. The results obtained demonstrated that active immunization against CG retarded significantly (P less than 0.01) the growth of the two transplantable tumors. Anti-CG antibodies were also determined and constantly found in the sera of all the preimmunized rats of both strains while no antibodies to CG were found in the control animals.
Accuracy of electromagnetic blood flow--and vascular diameter--measurements by means of intravascular loop probes in an extracorporeal alternating magnetic field can be impaired by an error signal induced in the probe stem. The standard method of removing this artifact by twisting the lead wires is difficult to implement in this case because the wires are bifilar and are made of highly resilient metals. The solution described here makes use of a hair pin loop incorporated within the probe stem in which an e.m.f. is induced that can be used to cancel the unwanted e.m.f. induced in the lead wires of the loop of the sensor. This scheme is applicable to simple loop probes as well as to orthogonal double-loop sensors.
The method of induction angiometry has been used for observation of active and passive venous vasomotion, without surgical exposure of the blood vessel. The diameter sensor is a resilient loop introduced into the vasculature through a fine No. 5 French (1 mm i.d.) angiographic catheter or a needle of comparable internal diameter. An extracorporeal a. c. magnet induces an electromotive force (e.m.f.) in the loop which acts as the secondary of a transformer, the electromagnet being the primary. Pulsations in the blood vessel diameter vary the loop area and with it the induced e.m.f. thus providing a linear measure of relative changes in vascular diameter. Changes in the order of 2 micra in a venous diameter of 5 mm can be resolved in-situ. Examples are given of registration of phasic venous diameter changes at the frequencies of the heart beat, respiration and Mayer waves. Pharmacological tests illustrate the ability to detect venous vasomotion in response to a dose below 0.1 microgram/kg of nitroglycerin in dogs.