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Biomedical subjects

J H Kalbfleisch

Publications and source records attributed to J H Kalbfleisch.

At least 37 records · Page 2Linked to original sources

Highly variable gastric emptying in patients with insulin dependent diabetes mellitus.

Some diabetic patients--particularly those with nausea and vomiting--frequently have evidence of delayed gastric emptying while other diabetic patients may in fact exhibit accelerated gastric emptying. Whether the presence or absence of symptoms of upper gastrointestinal dysfunction correlated with objective measures of gastric emptying in insulin dependent diabetic subjects was investigated. Twenty one insulin dependent diabetic patients underwent a solid phase gastric emptying scintiscan using in vivo labelled chicken liver. Thirteen patients had symptoms suggestive of gastrointestinal dysfunction (nausea, vomiting, early satiety, or constipation), while eight patients had no gastrointestinal symptoms. Eleven patients had orthostatic hypotension. All patients had been diabetic since childhood or adolescence. As a group, the diabetic patients showed a half time (T50) of gastric emptying (mean (SD) 150.0 min (163.7) that was not significantly different from that of 12 healthy control subjects (148.1 min (62.4)). Those diabetic patients without gastrointestinal symptoms and without orthostatic hypotension, however, showed a gastric emptying half time (70.1 min (41.6)) that was significantly faster than that of the control subjects. Conversely, those diabetic patients with nausea, vomiting, and early satiety (or early satiety alone) showed T50 values that were significantly greater than those of the diabetic patients without these symptoms. No correlation was found between the T50 value and the duration of diabetes, the fasting blood glucose at the time of study, or the respiratory variation in heart rate (E:I ratio). These observations indicate that highly variable rates of gastric emptying occur in insulin dependent diabetic patients, and that accelerated gastric emptying may occur in diabetic patients who have no symptoms of gastrointestinal dysfunction.

Adult↗

Investigation of the influence of acetylsalicylic acid on the steady state of long-term therapy with theophylline in elderly male patients with normal renal function.

The risk inherent in the clinical control of patients with theophylline is widely recognized. Elderly patients may present an additional risk because of altered pharmacokinetics and the use of concomitant medication. Acetylsalicylic acid has been proposed for primary and secondary prevention of myocardial infarction and possible strokes. This investigation was undertaken to determine if concomitant administration of acetylsalicylic acid in elderly patients would alter steady-state levels of theophylline. A population of smoking male patients older than 60 years of age under long-term control of chronic obstructive pulmonary disease (COPD) with theophylline were evaluated for a baseline period of 3 days. Serum levels were measured at 6:00 AM and 6:00 PM. An enteric-coated acetylsalicylic acid preparation, 650 mg by mouth, was added to the daily slow-release theophylline, 6:00 AM hour dose regimen for 4 weeks. The serum levels of theophylline and salicylates were measured at 6:00 PM after dosing and at 6:00 AM the following day, at weekly intervals for 4 weeks. Urine specimens collected before administration of medication at 6:00 AM were analyzed for salicylates to further confirm dosage compliance. All volunteers continued to be clinically controlled throughout the treatment period and no symptoms of either overdose or underdose of either medication occurred. Plateau or trough theophylline serum levels did not change significantly during the salicylate treatment period. Salicylate serum levels did show during treatment self-induced metabolism. It is concluded that in elderly male patients, a daily concomitant therapeutic salicylate regimen does not alter steady-state serum theophylline levels and therefore does not per se necessitate the assay of theophylline blood levels in elderly patients.

Aged↗

Proposed animal model of attention deficit hyperactivity disorder.

Dopamine (DA) neurons are implicated in the hyperlocomotion of neonatal 6-hydroxydopamine (6-OHDA)-lesioned rats, an animal model of attention deficit hyperactivity disorder (ADHD). Because serotonin (5-HT) neurons mediate some DA agonist effects, we investigated the possible role of 5-HT neurons on locomotor activity. Rats were treated at 3 days after birth with vehicle or 6-OHDA (134 micrograms ICV; desipramine pretreatment, 20 mg/kg IP, 1 h), and at 10 weeks with vehicle or 5,7-dihydroxytryptamine (5,7-DHT; 75 micrograms ICV; pretreatment with desipramine and pargyline, 75 mg/kg IP, 30 min), to destroy DA and/or 5-HT fibers. Intense spontaneous hyperlocomotor activity was produced in rats lesioned with both 6-OHDA and 5,7-DHT. Locomotor time in this group was 550 +/- 17 s in a 600 s session, vs. 127 +/- 13 s in the 6-OHDA group and < 75 s in 5,7-DHT and intact control groups (p < 0.001). Oral activity dose-effect curves established that 5,7-DHT attenuated DA D1 receptor supersensitivity and further sensitized 5-HT2c receptors. Acute treatment with dextroamphetamine (0.25 mg/kg SC) reduced locomotor time in 6-OHDA + 5,7-DHT-lesioned rats to 76 +/- 37 s (p < 0.001). Striatal DA was reduced by 99% and 5-HT was reduced by 30% (vs. 6-OHDA group). Because combined 6-OHDA (to neonates) and 5,7-DHT (to adults) lesions produce intense hyperlocomotion that is attenuated by amphetamine, we propose this as a new animal model of ADHD. The findings suggest that hyperactivity in ADHD may be due to injury or impairment of both DA and 5-HT neurons.

5,7-Dihydroxytryptamine↗

Increased prevalence of Helicobacter pylori antibodies among nurses.

BACKGROUND: Numerous studies have suggested that Helicobacter pylori infection in asymptomatic subjects is transmitted from person to person. Its prevalence is higher in the institutionalized setting. If that is the case, persons involved in patient care should have a higher prevalence of the infection. METHODS: We estimated the prevalence of H pylori antibodies among groups of asymptomatic medical and nursing staff and compared them with volunteer blood donors of similar age and sex. RESULTS: One hundred fifty-eight nurses and aides, 59 residents, 46 senior medical students, and 22 senior nursing students were enrolled in this study. Serum samples were tested for IgG antibodies against H pylori by enzyme-linked immunosorbent assay. Sixty-two (39%) of 158 nurses were found to be positive for antibodies to H pylori compared with 114 (26%) of 441 specimens from the blood donor group. Within the youngest age group (20 to 34 years), 13 (25%) of 51 nurses were positive for H pylori antibodies compared with 19 (13%) of 143 age-matched serum samples from the blood donor group. Within the middle age group (35 to 49 years), 32 (39%) of 83 nurses were positive for H pylori antibodies vs 43 (26%) of 167 age-matched blood donors. In the oldest age group (> 50 years), 17 (71%) of 24 nurses were positive for H pylori antibodies compared with 52 (40%) of 131 age-matched blood donors. Twenty-three (27%) of 86 nurses with 1 to 15 years of occupational exposure were positive for H pylori antibodies compared with 40 (56%) of 72 nurses with more than 15 years of occupational exposure. CONCLUSIONS: Nurses have an increased prevalence of H pylori antibodies that is significantly higher than the comparable prevalence of volunteer blood donors and is evident in the youngest age group. In addition, the increased prevalence is related to a longer duration of patient exposure in the nursing group.

Adult↗

Comparison of the pathogenicity of three species of coagulase-negative Staphylococcus in a mouse model with and without a foreign body.

Staphylococcus schleiferi, Staphylococcus lugdunensis, and Staphylococcus epidermidis produce a high incidence of abscesses in a mouse model with an implanted foreign body. We investigated the significance of the foreign body in this process. Fourteen strains of S. schleiferi, S. epidermidis, and S. lugdunensis were tested in our model. A preadhered foreign body was implanted into one mouse group, followed by injection of a test strain. Another group received injection without implant. Abscesses were assessed at 7 days; foreign bodies and infected tissues were cultured. The percent of samples that developed abscesses or were culture positive was compared for each strain. Nearly all mice infected with S. schleiferi developed abscesses and were culture positive. The foreign body made no difference in abscess formation for three of four S. schleiferi but increased the incidence of both organism recovery and abscess for three of five S. epidermidis. The foreign body enhanced abscess formation for four of five S. lugdunensis, with all five strains yielding significantly more culture recovery. Although the pathogenicity of nine strains was increased by the foreign body, five strains yielded high abscess and culture recovery rates that were not enhanced by its presence.

Abscess↗

Lipid peroxidation caused by hyperthermic perfusion of rat liver.

The data presented support the premise that hyperthermia-induced hepatocellular injury is the end result of lipid peroxidation. Evidence for lipid peroxidation is the formation of diene conjugates and the decrease in microsomal P450 and glucose-6-phosphatase activity during hyperthermic liver perfusion.

Animals↗

Randomized comparative study of cefixime versus cephalexin in acute bacterial exacerbations of chronic bronchitis.

Patients with purulent exacerbation of chronic bronchitis were randomized to receive either a single 400-mg daily dose of cefixime or 250 mg of cephalexin, orally, four times a day. Patients were males with a mean age of 63 years. Of the 86 patients, 71 (82%) had bronchitis caused by a single organism (29 by Haemophilus influenzae, 27 by Branhamella catarrhalis, 9 by gram-negative enteric organisms, 6 by Streptococcus pneumoniae), while more than one pathogen was implicated in 15 patients (18%). A total of 70.8% of the cefixime group and 50% of the cephalexin group were clinically cured (chi 2 = 3.89, P less than 0.05); however, when the categories of cured and improved were combined, no significant difference was noted between treatment groups (chi 2 = 3.39, P = 0.06). Analysis of side effects included all 130 evaluable and nonevaluable patients: diarrhea was noted in six patients in the cefixime group and none of the patients in the cephalexin group (P = 0.013 by the Fisher exact test). The diarrhea was mild and self-limited in all cases. B. catarrhalis has emerged as a major cause of exacerbation of bronchitis in our experience; there is an increased need to emphasize the examination of sputum samples by Gram staining if cost-effective antibiotic choices are to be made; any empirically chosen antibiotic should have activity against beta-lactamase-producing strains of B. catarrhalis as well as S. pneumoniae and H. influenzae.

Acute Disease↗

Pathogenicity of Staphylococcus lugdunensis, Staphylococcus schleiferi, and three other coagulase-negative staphylococci in a mouse model and possible virulence factors.

Staphylococcus lugdunesis and Staphylococcus schleiferi, two newly described species, have been isolated from numerous types of human infections. We compared the pathogenicity of 30 strains of S. lugdunensis, S. schleiferi, Staphylococcus epidermidis, Staphylococcus warneri, and Staphylococcus hominis, using a mouse model in which a foreign body preadhered with the test strain was implanted subcutaneously, followed by injection of the test strain. All five species of staphylococci produced abscesses. Staphylococcus epidermidis, S. schleiferi, and S. lugdunensis yielded species means of 76-91% abscess formation; 80-100% of the infected foreign bodies and tissues were culture positive. These three species were more virulent than S. warneri or S. hominis, which produced abscesses in 54 and 65% of mice, respectively; only 10-48% of the infected samples were culture positive. Transmission electron microscopy of pure cultures of selected strains showed that all species possessed glycocalyx. All species produced a variety of possible virulence factors, such as alpha and delta hemolysins, as well as the aggressins lipase and esterase. The production of exoenzymes did not always correlate with virulence as demonstrated by abscess formation in mice.

Abscess↗

Structural and functional characteristics of muscle from diabetic rodent small intestine.

After 30 days of streptozotocin-induced diabetes, the small intestine from untreated diabetic, insulin-treated diabetic, and nondiabetic rodents was excised in toto and measured. Despite a net loss in body weight, the diabetic animals showed a near twofold increase in small intestinal weight. This was characterized by a 148% increase in mucosal mass as well as a 39% increase in intestinal smooth muscle mass (P less than 0.05, respectively). The diabetic intestine was significantly longer and had a greater diameter and surface area. Diabetes significantly increased mucosal mass per unit surface area but produced an insignificant decrease in smooth muscle mass per unit surface area. Insulin treatment of the diabetic animals prevented the increase in total mucosal mass and mucosal mass per unit surface area. Insulin treatment also prevented the increase in smooth muscle mass, but reduced smooth muscle mass per unit surface area to a level significantly less than that found in nondiabetic intestine. In vitro dose-response studies of circular and longitudinal small intestinal muscle from the diabetic animals showed normal tension development and sensitivity to both bethanechol chloride and physostigmine. These observations show that the diabetic state produces alterations in not only mucosal but also smooth muscle mass in the small intestine. However, despite these morphological changes, diabetic intestinal smooth muscle retains its sensitivity to cholinergic stimulation and its capacity for tension generation.

Animals↗

Effect of increased central blood volume with water immersion on plasma catecholamines during exercise.

To examine the influence of an increase in central blood volume with head-out water immersion (WI) on the sympathoadrenal response to graded dynamic exercise, nine healthy men underwent upright leg cycle exercise on land and with WI. Plasma norepinephrine and epinephrine concentrations were used as indexes of overall sympathoadrenal activity. Oxygen consumption (VO2), heart rate, systolic blood pressure, and plasma concentrations of norepinephrine, epinephrine, and lactate were determined at work loads corresponding to approximately 40, 60, 80, and 100% peak VO2. Peak VO2 did not differ on land and with WI. Plasma norepinephrine concentration was reduced (P less than 0.05) at 80 and 100% peak VO2 with WI and on land, respectively. Plasma epinephrine and lactate concentrations were similar on land and with WI at the three submaximal work stages, but both were reduced (P less than 0.05) at peak exertion with WI. Heart rate was lower (P less than 0.05) at the three highest work intensities with WI. These results suggest that the central shift in blood volume with WI reduces the sympathoadrenal response to high-intensity dynamic exercise.

Adrenal Glands↗

Effects of hyperthermia on xanthine oxidase activity and glutathione levels in the perfused rat liver.

The hepatotoxic effects of hyperthermic liver perfusion were investigated in male Fischer 344 rat livers. Perfusions were carried out at 37, 41, 42, 42.5, and 43 degrees C for 2 hr. During the 2 hr, the perfusate was analyzed for activity of aspartate aminotransferase (AST), lactate dehydrogenase (LDH), N-acetyl-beta-glucosaminidase (NAG), and glutathione (GSH), oxidized glutathione (GSSG), allantoin, and potassium. After perfusion, each liver was homogenized and analyzed for total xanthine oxidase (XO) activity, percentage type-D and type-O XO, and total GSH content. Perfusate AST, LDH, NAG, and potassium levels were increased significantly with time and were significantly different in all hyperthermic perfusions from the 37 degrees C perfusion values by the end of the perfusion. Perfusate GSH + GSSG levels were increased significantly in all hyperthermic perfusions after 60 min. Liver GSH levels were significantly lowered following perfusion at hyperthermic temperatures. There was a temperature-dependent increase in the percentage of XO in the type-O form following perfusion at hyperthermic temperatures, which was strongly and positively correlated with the loss of hepatic GSH. These data support the hypothesis that hyperthermic toxicity to the liver is the result of oxidative stress brought about by conversion of XO to the type-O form.

Acetylglucosamine↗

Hyperthermic liver toxicity: a role for oxidative stress.

Rat livers were perfused at 37 degrees C, 41 degrees C, 42 degrees C, 42.5 degrees C, and 43 degrees C for 2 hr. Among perfusate constituents analyzed were urea, total amino acids, N-acetyl-beta-glucosaminidase (NAG), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), malonaldehyde (MDA), glutathione (GSH), oxidized glutathione (GSSG), allantoin, potassium, phosphate, and glucose. After perfusion, livers were homogenized and analyzed for xanthine oxidase (XO) activity, GSH content, and lysosomal lability. Perfusate AST, LDH, NAG, potassium, glucose, and phosphate increased significantly with time, and there were significant differences in the final values between 37 degrees C and 42 degrees C, 42.5 degrees C and 43 degrees C (P less than .05). GSH levels increased significantly at all temperatures after 90 and 120 min, whereas GSSG levels differed significantly at 60, 90, and 120 min for 37 degrees C vs. 42 degrees C, 42.5 degrees C, and 43 degrees C (P less than .05). Mean MDA levels at 37 degrees C differed from those at 41 degrees C and 43 degrees C (P less than .05) at each temperature. Allantoin levels increased significantly with time of perfusion; mean levels at 37 degrees C were significantly different from mean levels at each temperature at 60, 90, and 120 min. GSH liver tissue levels decreased with perfusion at hyperthermic temperatures; mean values at 41 degrees C, 42 degrees C, and 42.5 degrees C, and 43 degrees C differed from 37 degrees C mean values (P less than .01). Type O XO increased after 120 min perfusion from 6.4% +/- 2.0% at 37 degrees C to 55% +/- 30%, 43% +/- 27%, and 63% +/- 29% at 42 degrees C, 42.5 degrees C, and 43 degrees C, respectively. Lysosomal lability increased after perfusion at 42.5 degrees C. There was a significant increase in nonsedimentable NAG activity at 42.5 degrees C (P less than .05). These data support the premise that hyperthermic toxicity to the liver may be a consequence of oxidative stress brought about by enhanced adenosine triphosphate (ATP) consumption and conversion of XO to type O. Such conversion results in superoxide formation and subsequent depletion of cellular GSH, labilization of the lysosomes, and plasma membrane damage.

Allantoin↗

Evidence for muscarinic inhibitory neurotransmission in rodent small intestine.

The influence of cholinergic and noncholinergic inhibitory nerves was examined in circular and longitudinal muscle from the duodenum. Rodent proximal small intestine was cut into strips measuring 6.0 x 10.0 mm. Strips cut along the oral-caudal axis were called longitudinal strips, whereas those cut 90 degrees to that axis were called circular strips. The strips were stretched to their optimal lengths and subjected to electrical field stimulation in the presence of various concentrations of atropine, pirenzepine or McN-A-343-11. All three drugs inhibited field-stimulated contraction responses and produced or augmented relaxation responses in both muscle layers. All relaxation responses were abolished by tetrodotoxin, indicating they were due to excitation of inhibitory nerves. For each response examined atropine was significantly more potent than pirenzepine (relative potency ratio, 13.36-95.74). The inhibitory effect of McN-A-343-11 on longitudinal muscle was antagonized by both atropine and pirenzepine, indicating the recruitment of cholinergic inhibitory nerves. Neither atropine nor pirenzepine had any effects on inhibitory responses produced by McN-A-343-11 in circular muscle, indicating the recruitment of noncholinergic inhibitory nerves. McN-A-343-11 also increased spontaneous contraction amplitudes in both muscle layers by a direct (tetrodotoxin-resistant) effect on smooth muscle. This effect was also antagonized by atropine and pirenzepine. Thus, both cholinergic and noncholinergic nerves participate in inhibitory neuromuscular transmission in the small intestine. Circular muscle is dominated by a noncholinergic inhibitory innervation. Longitudinal muscle appears to be controlled by both cholinergic and noncholinergic inhibitory nerves.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗

Comparison of ST segment depression in upright treadmill and supine bicycle exercise testing.

Significant differences in the hemodynamic response to upright and supine exercise have been reported in patients with coronary artery disease. The purpose of the present study was to compare the degree of myocardial ischemia as assessed by ST segment depression during upright treadmill and supine bicycle exercise in 98 patients with coronary artery disease and in 34 patients with normal coronary arteries. The amount of ST segment depression at maximal exercise in patients with coronary artery disease was 0.90 +/- 0.80 mm for treadmill and 1.34 +/- 1.09 mm for supine bicycle (p less than 0.001). The amount of ST segment depression during treadmill and supine bicycle exercise tests was also compared at highest similar heart rates (0.68 +/- 0.77 versus 1.17 +/- 1.01, p less than 0.001), at highest similar rate-pressure products (0.71 +/- 0.77 versus 1.08 +/- 1.04, p less than 0.001), at highest similar metabolic equivalents of oxygen consumption (MET) levels (0.69 +/- 0.75 versus 1.20 +/- 1.05 mm, p less than 0.001) and at the onset of angina (0.84 +/- 0.73 versus 1.18 +/- 0.88 mm, p less than 0.001). The rate-pressure product achieved at maximal exercise was similar in both tests (18.74 +/- 5.80 x 10(3) versus 18.81 +/- 5.17 x 10(3), p = NS). The occurrence of angina during treadmill and supine bicycle exercise tests was similar (47 of 98 versus 48 of 98, respectively, p = NS). For the detection of coronary artery disease, the sensitivity was 50.0% for treadmill and 63.3% for supine bicycle (p less than 0.05) and the specificity was 73.5 versus 70.6%, respectively (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Volatile anesthetics attenuate sympathomimetic actions on the guinea pig SA node.

The authors examined and compared the direct effects of three volatile anesthetic agents and three sympathomimetic agonists on transmembrane action potential (AP) characteristics and automaticity of sinoatrial (SA) nodal pacemaker cells. SA nodal tissue was isolated from guinea pig hearts and suffused in vitro with oxygenated Krebs-Ringer solution. Electrophysiologic variables measured were: amplitude of the AP, slopes of phase 4 and of phase 0 of the AP, AP duration, and spontaneous sinus rate. The authors found that 1 and 2 MAC equivalents of each anesthetic, 0.8 and 1.6 vol % halothane, 1.4 and 2.8 vol % isoflurane, and 1.7 and 3.4 vol % enflurane similarly depressed the slopes of phase 4 and 0 of the AP, prolonged AP duration, and slowed the sinus rate at 1 and 2 MAC equivalents. Isoproterenol, 0.25 microM, and epinephrine, 50 microM, maximally enhanced the slopes of phase 4 and 0 of the AP, shortened AP duration, and increased the sinus rate, but phenylephrine, 50 microM, only moderately increased the slope of phase 4 and the sinus rate. Each of the three anesthetics caused baseline depressions of phase 4 and phase 0 slopes and of automaticity of SA nodal cells; the fall in sinus rate was counteracted, but was not reversed maximally by increasing the concentrations of isoproterenol, epinephrine, or phenylephrine. Regression analyses of linearly transformed data showed that each of the anesthetics similarly depressed basal sinus rate, so that changes in rate produced with isoproterenol and epinephrine were not different from those observed with beta agonists in the absence of anesthetics.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

Distribution of excitatory junction potential amplitude in cat cerebral arteries: examination of its quantal nature and modulation by opiates.

We used scorpion venom to release small amounts of an excitatory neurotransmitter from adventitial nerves in cat left anterior descending cerebral artery. We used glass microelectrodes to measure and record postsynaptic electrical events of minimal amplitude. These events were similar to postsynaptic spontaneous and electrically evoked excitatory junction potentials (ejp's) seen in skeletal muscle. We performed a frequency analysis of the ejp amplitudes to determine if they fit a unimodal or multimodal distribution. We also investigated the effects of phentolamine, norepinephrine, hydromorphone, and morphine on ejp amplitude and frequency in the artery. Statistical analysis of the ejp frequency and amplitude revealed a multipeaked distribution with decreasing peaks. These results were similar to the distribution reported for acetylcholine release in skeletal muscle. The ejps were inhibited by phentolamine, which suggested that these events were adrenergically mediated. Norepinephrine and the opiates, hydromorphone and morphine, reduced the frequency and amplitude of the ejp's. The vessels also constricted to increasing doses of norepinephrine both under control conditions and in the presence of opiate. These results suggest that norepinephrine blocks the ejp's by a feedback mechanism at the presynaptic membrane and that endorphins and/or enkephalins, also acting at this presynaptic site, may modulate neurotransmission in the cerebral circulation.

Animals↗

Circulating IgG antibodies against fungal and actinomycete antigens in the sera of farmer's lung patients from different countries.

Sixty-nine farmer's lung patients and 28 normal controls from four countries (Finland, Switzerland, Canada and the United States) were investigated for antibody levels against 13 antigens commonly used for the screening panel for hypersensitivity pneumonitis. Of these antigens, eight were from the Medical College of Wisconsin (United States) and five were from the University of Kuopio (Finland). IgG antibodies against these antigens were studied in 97 sera using a sensitive biotin-avidin-linked enzyme immunoassay. The results indicate that the mean antibody titer against Micropolyspora faeni was highest in the United States (U.S.) followed by Finland. Both Finnish and U.S. antigens reacted almost identically against various groups of patients, although the degree of reactivity varied considerably. Higher antibody levels against Thermoactinomyces vulgaris were detected in Finnish patients than patients from other countries while patients from all four countries showed elevated levels of antibodies against T. candidus. This study demonstrates that antigens from identical species, irrespective of geographic origin, reacted similarly. However, variability between antigens of the same species was still considerably significant. Since the microbiological flora of moldy hay varies widely in different regions, the microbial species associated with the disease at a given geographical area has to be determined before selecting antigens for serological studies. The antigens currently used in various laboratories are crude preparations and need to be purified and standardized for dependable results. Until such antigens are available, all antigenic preparations used in the immunological evaluation of patients should be immunochemically characterized for their reproducibility and reliability although the ultimate goal should be to obtain standardized pure antigens for dependable immunodiagnosis of farmer's lung.

Antibodies, Bacterial↗