The effect of Pseudomonas NCIMB 2021 biofilm on AISI 316 stainless steel.

A bioreactor system operating in a continuous mode was designed to generate biofilms on polished and as-received surfaces of AISI 316 stainless steel coupons exposed for 36 d to a pure culture of marine Pseudomonas NCIMB 2021. Scanning electron microscopy (SEM) and atomic force microscopy were employed to determine the degree of surface colonisation and to examine corrosion damage of the steel. X-ray photoelectron spectroscopy analysis was carried out to characterise the chemistry of the passive layers on polished steel stored for a period of time, freshly re-polished coupons, and as-received steel. The effect of biofilms on the composition of layers formed on the steel specimens was evaluated. SEM revealed that the surfaces of polished and stored steel appeared to accumulate more biofilm compared to as-received specimens. Micropitting of steel occurred underneath the biofilm, regardless of surface finish. The concentration of elements in the passive layers differed significantly between freshly re-polished and as-received or polished and stored coupons. In the presence of Pseudomonas NCIMB 2021 biofilm, the composition of the passive layer on the as-received steel surface was considerably altered compared to unexposed steel or steel exposed to abiotic medium.

The effect of extracellular polymeric substances on the attachment of Pseudomonas NCIMB 2021 to AISI 304 and 316 stainless steel.

Surfaces of AISI 304 and 316 stainless steels were pre-treated with three different types of extracellular polymeric substances, viz. (i) exopolymers released into the culture medium ("free"; or planktonic exopolymers), (ii) capsular exopolymers, and (iii) biofilm exopolymers, produced by continuous cultures of marine Pseudomonas NCIMB 2021. The initial attachment of Pseudomonas cells to exopolymer-conditioned steel surfaces varied with the exopolymer type and concentration. Results gained from wettability studies of exopolymer-treated steel using contact angle measurements, as well as from the surface roughness measurements conducted employing atomic force microscopy analysis, could not account for the observed, statistically significant differences (p < 0.1) in the level of bacterial surface colonisation. It is therefore proposed that neither surface hydrophobicity nor roughness play an important part in the early attachment of Pseudomonas NCIMB 2021 to the conditioned steel surfaces and that a difference in the chemistry of the exopolymers is most likely a key parameter influencing initial cell adhesion to pre-treated steel.

Study of the interaction of sulphate-reducing bacteria exopolymers with iron using X-ray photoelectron spectroscopy and time-of-flight secondary ionisation mass spectrometry.

Time-of-flight secondary ionisation mass spectrometry and X-ray photoelectron spectroscopy were employed to determine the interaction of crude extracellular polymeric substances recovered from static batch cultures of two isolates of marine sulphate-reducing bacteria of the genus Desulfovibrio, grown in the presence of and without mild steel surfaces, with Fe ions released from steel. The results demonstrated that exopolymers synthesised by different strains of sulphate-reducers varied in their ability to bind iron originating from steel. Based on the X-ray photoelectron spectroscopy analysis it is proposed that Fe released from steel was associated with bacterial exopolymers such as Fe(III) ion. The application of surface science techniques to study exopolymer/metal interaction allowed quantitative evaluation of Fe binding using small sample size.

Lipoinjection as a treatment of pacemaker pocket neuralgia.

Chronic severe pacemaker pocket neuralgia secondary to inadequate subcutaneous tissue between the pacemaker and overlying skin typically is treated by surgical pocket revision or relocation of the system. A case of this complication successfully treated by lipoinjection is reported. Additional experience is needed to confirm the usefulness of the technique as a means of providing symptomatic relief without the risks associated with more invasive procedures.

The heart (ventricle and atrium) is the heart of hypertension, not blood pressure.

Some old icons of hypertension warrant questioning in view of new insights. Lowering of blood pressure is no criterion of efficacy in prevention of cardiovascular morbidity, mortality and sudden death. The drugs used in early studies - diuretics, vasodilators and reserpine - greatly improved mortality from malignant hypertension, apoplectic stroke and congestive heart failure, but had little or no effect in persons with milder degrees of elevated blood pressure, who constitute the vast majority of hypertensives. The failure of diuretics and vasodilators to influence cardiovascular disease favorably appears due not to their known adverse effects on risk factors, such as lipids, as some have held, but to a failure - in conjunction with some sympathetic blocking agents - to cause effective regression of left ventricular hypertrophy, the keystone of successful therapy. A study of 674 hypertensive persons surveyed in the United States and eastern Canada, personally examined during their visit to a Florida health resort, has shown striking changes in prescribing practice during the period surveyed (1985-88), notably with increased use of angiotensin converting enzyme (ACE) inhibitors and, to a lesser degree, increased use of calcium channel blockers. Both of these cause regression of left ventricular hypertrophy, and will hopefully show long term benefit in decreasing hypertension mortality. Left ventricular hypertrophy is detected most sensitively echocardiographically, and is worthwhile not only for estimation of prognosis, but also for guiding therapy. Left atrial hypertrophy is a mirror of left ventricular hypertrophy and may be detected echocardiographically and in the electrocardiogram.(ABSTRACT TRUNCATED AT 250 WORDS)

Major new developments affecting treatment and prognosis in hypertension.

Joint studies of the ALIMDA and Society of Actuaries, notably those of 1935, 1959 and 1979, established that there is a progressive rise in cardiovascular mortality with successive increments in blood pressure. This has provided the basis of underwriting. The converse is not true, or at least has not been true until very recently. Drugs that effectively reduce blood pressure have been available for several decades, but reduction and maintenance of blood pressure is still accomplished in only a minority of hypertensives. Long-term trials employing a combination of drugs, i.e., diuretics, vasodilators and reserpine and subsequently beta-blockers, almost without fail have not shown that treatment with these agents significantly reduces heart disease mortality and sudden death. This has been attributed, perhaps without basis, to an unfavorable countering effect of increased lipid levels, aggravating this risk factor, and other undesirable metabolic effect of diuretics, such as hypokalemia and depletion of body magnesium, increasing the propensity to ventricular arrhythmias, hyperglycemia, worsening diabetes, and hyperuricemia. A survey of 674 persons with hypertension seen personally during the period 1985-89, who were under the care of approximately that many physicians, reveals striking changes in drug prescription and use during this brief period that portend a major change in the outlook of hypertension. Two classes of drugs have increased rapidly in popularity: these are the angiotensin-converting enzyme inhibitors (ACE inhibitors) and the calcium blockers. Both classes of drugs effectively lower blood pressure and have minimal side effects with good compliance. They act not only to reduce peripheral vascular resistance, but also locally in the heart muscle to directly cause left ventricular hypertrophy to regress, an effect of great consequence. The drugs used in former trials such as the vasodilators and diuretics have no effect on left ventricular hypertrophy, unlike the ACE inhibitors and calcium antagonists. Left ventricular hypertrophy is the key lesion in hypertension and is only in part due to increased work load imposed by elevated pressure. It is associated with elevated blood pressure, but not closely and occurs independently; ventricular myocytes as well as myocytes of the vasculature being stimulated to growth by angiotensin and calcium, potentiating the effect of norepinephrine. Left ventricular hypertrophy greatly increases the propensity to ventricular arrhythmias and sudden death, and is a prime cause of cardiac mortality and sudden death not only in hypertension, but also in obesity, aging and diabetes, in which conditions left ventricular hypertrophy also is very common.(ABSTRACT TRUNCATED AT 400 WORDS)

Effect of "aminopterin" on epithelial tissues.

The folic acid antagonist, 4-aminopteroyl glutamic acid ("aminopterin"), is a potent inhibitor of growth and of connective tissue proliferation. The present study indicates that the suppressive effects of "aminopterin" on epithelial structures are more striking than on connective tissue, as revealed by observation of interference with wound healing and epithelization, atrophy and ulceration of mucosa, alopecia, and prompt suppressive effects in such dermatologic disorders as psoriasis and chronic indurative dermatoses. "Aminopterin" was administered orally in daily doses of 1.5 to 2.0 mg. to thirteen patients with psoriasis (of whom six had associated arthritis) and to five patients with chronic indurative dermatoses. The latter included one patient with chronic atopic eczematoid dermatitis with associated asthma, one with chronic eczematoid seborrheic dermatitis, one with chronic discoid lupus erythematosus involving the face, and two with scleroderma. In all patients there were remissions in cutaneous lesions, which appeared most commonly between the 5th and 10th day of "aminopterin" therapy. Treatment was interrupted in most patients after an initial course of 14 to 28 mg. because of the regular occurrence of shallow ulceration of the buccal mucosa and frequent development of abdominal cramps. Remissions persisted for periods ranging from two weeks to several months, after which lesions returned which responded to further courses of "aminopterin." The therapeutic response was more complete in the seven patients with psoriatic arthritis than in in six subjects with uncomplicated psoriasis. In four patients with psoriatic arthritis in whom the responses to "aminopterin" and cortisone were compared, arthritic manifestations were considerably more relieved by cortisone, but improvement in psoriasis was consistently more complete and more sustained with "aminopterin." No evidence of a summative effect of cortisone and "aminopterin" on psoriasis was observed when the two were employed concomitantly, although amelioration of arthritic symptoms was more complete than when cortisone was given alone. Topical application of "aminopterin" in a 1% ointment was found to be ineffective. "Aminopterin" is a toxic drug, and its administration must be carefully supervised. The citrovorum factor has proved useful in overcoming "aminopterin" toxicity but interferes with its therapeutic effects. It is suggested that "aminopterin" may prove useful in other dermatologic disorders and in cutaneous manifestations of some systemic diseases which, in certain instances, have been temporarily benefited by cortisone.

Introduction of antifolics in psoriasis. A twenty-five year retrospect of antineoplastic agents in nonmalignant disease.

Presented herein is a review of the beneficial use of the folic acid antagonist, aminopterin, in the treatment of psoriasis and other dermatologic disorders.