Biomedical subjects
Publications and source records attributed to A Pawlowicz.
A study of the oral health of workers in flour mills was carried out. The examined group consisted of 40 males and 8 females currently employed at flour mills. As much as 93.75% of the workers showed evidence of dental abrasion, particularly of the front teeth. The authors concluded that the dental abrasions in the group are closely related to the work environment.
The initiator of coliphage lambda DNA replication, lambda O protein, may be detected among other 35S-labeled phage and bacterial proteins by a method based on immunoprecipitation. This method makes it possible to study lambda O proteolytic degradation in lambda plasmid-harboring or lambda phage-infected cells; it avoids ultraviolet (u.v.)-irradiation of bacteria, used for depression of host protein synthesis, prior to lambda phage infection. We confirm the rapid decay of lambda O protein (half-time of 80 s), but we demonstrate the existence of a stable lambda O fraction. In the standard five minute pulse-chase experiments, 20% of synthesized lambda O is stable. The extension of the [35S]methionine pulse, possible in lambda plasmid-harboring cells, leads to a linear increase of this fraction, as if a part of the synthesized lambda O was constantly made resistant to proteolysis. Less than 5% of lambda O protein synthesized during one minute is transformed into a stable form. We presume that the stable lambda O is identical with lambda O present in the normal replication complex and thus protected from proteases. We cannot find any stable lambda O in Escherichia coli recA+ cells that were irradiated with u.v. light prior to lambda phage infection, but their recA- counterparts behave normally, suggesting that recA function interferes in the assembly of a normal replication complex in u.v.-irradiated bacteria. The stable lambda O found in lambda plasmid-harboring, amino acid-starved relA cells is responsible for the lambda O-dependent lambda plasmid replication that occurs in this system in the absence of lambda O synthesis. The existence of stable lambda O raises doubt concerning its role as the limiting initiator protein in the control of replication. Another significance of lambda O rapid degradation is proposed.
Inhalation and nasal aspirin challenge has been investigated in asthma patients with co-existing rhinitis. Eight of 39 asthma patients were diagnosed as aspirin-sensitive on the basis of inhalation challenge. Seven aspirin-sensitive asthmatics were subjected to nasal aspirin provocation. During nasal challenge, all seven patients experienced a fall in FEV1 of at least 15%, two showed a significant increase (greater than 400%) in nasal airways resistance (NAR) and one developed urticaria. No significant changes in FEV1 or NAR were observed in nine normal subjects after aspirin inhalation and nasal challenge. There were no significant changes in FEV1 or NAR in six aspirin-tolerant asthmatics when aspirin was given intranasally. The results of this study show that aspirin nasal provocation impairs lung function in aspirin-sensitive asthmatics. In comparison with inhalation challenge responses are generally milder and easier to control. Nasal challenge is also less time-consuming than other methods of aspirin challenge and is therefore more suitable for routine use.
The in vitro release of endogenous and exogenous PgF2 alpha from plasma and serum proteins by aspirin and other analgesic drugs has been studied by RIA and equilibrium-dialysis techniques, respectively. Before aspirin addition, the mean plasma level of PgF2 alpha measured by RIA was significantly lower in aspirin-sensitive asthma (ASA) patients (11.3 +/- 6.5 pg/ml; n = 8) than in aspirin-tolerant asthma (ATA) patients (25.0 +/- 11.4 pg/ml; n = 21). After aspirin addition (50 micrograms/ml) the mean PgF2 alpha level detected in plasma by RIA was higher in ASA patients (97.6 +/- 5.5 pg/ml) than in ATA patients (66.9 +/- 4.5). The binding of [3H]PgF2 alpha to serum protein was significantly inhibited by NSAIDs but not by paracetamol (0.2-1.0 mM). These results implicate PgF2 alpha and the protein-binding property of analgesic drugs in the pathogenesis of aspirin-sensitive asthma.
In patients with aspirin-sensitive asthma, no significant changes in plasma beta-thromboglobulin or bicyclic prostaglandin (PG) E2 were observed during aspirin challenge. The addition of aspirin to platelet suspensions from patients with aspirin-sensitive asthma produced no detectable chemiluminescence. Small concentrations of aspirin generated PGF2 alpha but not PGE2 or PGD2 from plasma in vitro. PGF2 alpha levels were significantly higher in plasma from aspirin-sensitive patients and distinguished aspirin-sensitive from aspirin-tolerant patients with asthma. The results of this study suggest that the displacement of protein-bound PGF2 alpha may be of importance in the pathogenesis of aspirin-induced asthma.
A number of food additives and industrial chemicals, responsible for inducing symptoms of intolerance in some individuals, have been studied in tests measuring platelet activation by noradrenaline. All the investigated agents inhibited platelet aggregation and this was associated with inhibition of the cyclo-oxygenase-thromboxane pathway. Suboptimal inhibitory concentrations of the agents studied had additive inhibitory effects on platelet aggregation when they were tested in pairs, or when tested with salicylate or aspirin. The results support the theory that some food additives and industrial chemicals induce intolerance because of their aspirin-like properties.
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The subpleural blebs found in patients with so-called idiopathic spontaneous pneumothorax suggest that pneumothorax could possibly be an early manifestation of pulmonary emphysema in these subjects. In order to investigate this hypothesis, fifty-six young adults (32 +/- 9 yr; 45 men and 11 women) were examined after idiopathic spontaneous pneumothorax. All were apparently healthy with no history of pulmonary disease. Physical and X-ray examination were normal. The episode of pneumothorax was the only sign of lung pathology. A control group of 20 healthy people was also studied. The mean age and smoking habits in the patients and control groups were similar. Only four patients (7%) revealed definite evidence of emphysema, consisting of a reduction of diffusing capacity, decrease of lung recoil pressure and a secondary reduction of forced expiratory flow at 50% of vital capacity. Serum alpha-1-antitrypsin levels in these patients were normal.
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