Volatile compounds and antioxidative activity of Porophyllum tagetoides extracts.

Porophyllum tagetoides is an annual warm-weather herb that has an intense typical smell. Its leaves are commonly used in soup preparation and traditional medicine for treatment of inflammatory diseases. Its volatile compounds and antioxidant properties were evaluated in crude, aqueous and ethanol leaf extract and an oil emulsion using different antioxidant assays in vitro, such as: DPPH radical scavenging activity, redox potential, polyphenol content, reducing power and optical density. A high antioxidative activity was found when comparing leaves with stems. The crude extract from leaves showed a very high reducing power (2.88 ± 0.20 O.D.) and DPPH radical-scavenging activity (54.63 ± 4.80%), in concordance with a major concentration of vitamin C (23.97 ± 0.36 mg/100 g). Instead, the highest polyphenol content (264.54 ± 2.17 mg GAE/g of sample) and redox potential (561.23 ± 0.15 mV) were found by the ethanol and aqueous extract, respectively. Aldehydes and terpenes such as nonanal, decanal, trans-pineno, ß-myrcene and D-limonene were the major volatiles found. This study suggests that Porophyllum tagetoides extracts could be used as antioxidants.

First Report of Leaf Rust of Blueberry Caused by Thekopsora minima in Mexico.

Blueberry (Vaccinium corymbosum L.) is becoming an important crop in the states of Jalisco and Michoacan in Mexico. Leaf rust, a disease causing extensive defoliation on plants with severe infections, was observed in the autumn of 2007 and it has become one of the most significant diseases of blueberry in these states. Symptoms on the upper surfaces of leaves appear as small, yellow spots that later turn necrotic as they enlarge and coalesce and eventually cover large areas of individual leaves. On the undersides of leaves, small flecks surrounded by small water-soaked halos appear, turn yellow, and produce powdery sori that are uredinia with urediniospores. Uredinia were hypophyllous, scattered to gregarious and at times superficially appearing confluent, up to about 300 µm in diameter, dome shaped and peridium hemispherical in cross section, orangish, becoming pulverulent, lacking obviously enlarged, well-differentiated ostiolar cells. Urediniospores were subglobose, obovate, oblong or ellipsoid, 17.6 to 27.2 × 12.8 to 17.6 µm, with hyaline, echinulate walls that are 1.2 to 1.8 µm thick, and with yellow-to-hyaline contents. Telia were not observed. On the basis of uredinial morphology (3,4), the rust was identified as Thekopsora minima P. Syd. & Syd. To distinguish this rust from other rust species causing disease on Vaccinium (2,3), a 1,414-bp region consisting of ITS2 and the 5' end of the 28S was amplified with primers Rust2inv/LR6 from uredinial lesions on infected leaves of V. corymbosum 'Biloxi' and sequenced (BPI 880580; GenBank Accession No. HM439777) (1). Results of a BLAST search of GenBank found 100% (1,414 of 1,414) identity to T. minima (GenBank Accession No. GU355675) from South Africa (3). Pathogenicity tests were completed as follows: (i) during the autumn of 2009, rusted leaves of cvs. Biloxi and Sharpblue were collected from the field; (ii) mature leaves from healthy plants of both blueberry cultivars were surface disinfested with 1% sodium hypochlorite for 2 min and rinsed with sterile distilled water; (iii) fresh urediniospores from rusted leaves were brushed directly onto the undersides of disinfested detached leaves; (iv) to avoid drying, wet cotton balls were placed on the petioles of inoculated leaves that were subsequently placed in resealable plastic bags; and (v) leaves were then incubated in a growth chamber at 22°C with a 12-h photoperiod. For each cultivar, 20 leaves were inoculated and five uninoculated leaves were included as controls and the test was repeated once. Yellow uredinia were observed 13 and 10 days after inoculation in cvs. Biloxi and Sharpblue, respectively. Leaf symptoms and uredinial characters were the same as observed previously in the field. To our knowledge, this is the first report of T. minima in Mexico. This report is significant for growers who need a diagnosis to control the disease and for breeders and plant pathologists who should consider developing more resistant cultivars. References: (1) M. C. Aime. Mycoscience 47:112, 2006. (2) F. L. Caruso and D. C. Ramsdell, eds. Compendium of Blueberry and Cranberry Diseases. The American Phytopathological Society, St. Paul, MN, 1995. (3) L. Mostert et al. Plant Dis. 94:478, 2010. (4) P. Sydow and H. Sydow. Monographia Uredinearum. Vol. III. Fratres Borntraeger, Leipzig, Germany, 1915.

Factors associated with premature chromosome condensation (PCC) following in vitro fertilization.

From January 1989 to July 1990 a total of 562 oocytes was fixed in our In Vitro Fertilization Program, while cytogenetic data were collected in the case of 433. Forty-eight of these (11%) had a set of oocyte chromosomes in metaphase II, and at least one other set of sperm chromosomes prematurely condensed in the form of single chromatids. In the literature this phenomenon, frequent in our experience, has not been separately studied by many authors. Comparative studies with diverse parameters have shown a significant correlation between the same phenomenon and the use of follicle-stimulating hormone supplementation in ovarian stimulation protocols. Also, in some cases we found a high percentage of repetition of the phenomenon in one patient.

Selegiline use to prevent progression of Parkinson's disease. Experience in 22 de novo patients.

To test the hypothesis that selegiline (L-deprenyl), a selective inhibitor of B-type monoamine oxidase, can halt the natural progression of Parkinson's disease, its use in 22 naive patients (mean age, 58 years; mean Parkinson's disease duration, 2.3 years) in the early stages (1 to 2) of the disease was studied. Patients were started and maintained on a daily dose of 10 mg of selegiline, and they underwent neurologic examinations at 3-month intervals using our center's disease staging and total rated disability scores. The criterion set for disease progression was defined as either the appearance of a new objective sign and/or a definite, persistent worsening (greater than 25%) of existing signs after the initiation of the selegiline trial. Patients remained on a regimen of selegiline [corrected] for periods ranging from 7 to 84 months. At the time of their latest neurologic examination, 17 (77%) of the 22 patients had conditions that demonstrably worsened with selegiline alone at an average of 10.8 months from the start of the drug therapy. Six of these 17 patients with worsening conditions (or 27% of the original 22) eventually required the addition of levodopa with carbidopa (Sinemet) on average at 13 months from the start of selegiline therapy; they have continued, to date, taking this combination for an additional mean follow-up period of 20.7 months. Four of the original 22 patients had relatively unchanged, stable neurologic status at the time of their latest examination (average follow-up period, 11.6 months).(ABSTRACT TRUNCATED AT 250 WORDS)

Selegiline as an adjunct to conventional levodopa therapy in Parkinson's disease. Experience with this type B monoamine oxidase inhibitor in 200 patients.

Two hundred patients at a median age of 63 years, receiving conventional levodopa therapy for 8 years, who had had Parkinson's disease for 10 years, tried a regimen of selegiline (L-deprenyl), a type B monoamine oxidase inhibitor, at a daily dose of 10 mg, for varying periods from less than 6 months to more than 24 months (28% over 24 months). Selegiline does improve parkinsonism during the initial 6 months to 12 to 24 months of combined therapy in one third to almost half of patients with an end-of-dose type of response to long-term levodopa therapy. However, even this particular class of patients is unable to maintain such an improvement by 36 months, much less by 48 months, from the start of the selegiline trial. About one quarter of poor responders to levodopa and those with random deterioration show improvement in their parkinsonian status in the first 6 months of the selegiline trial, but their conditions quickly deteriorate by 1 year. The predominant pattern of response to previous levodopa therapy and the severity of the total disability score at the initiation of the selegiline trial were the two variables that were predictive of risk of failure with the drug. No evidence suggested that selegiline decreases the excess mortality rate of Parkinson's disease above that achieved with the use of levodopa alone. Selegiline as an adjunctive agent to conventional levodopa therapy was not unduly impressive with regard to preventing progression of Parkinson's disease.

Treatment of Parkinson's disease in early and late phases. Use of pharmacological agents with special reference to deprenyl (selegiline).

There are at present numerous pharmacological agents available for the control of parkinson symptoms. None are ideal; all have their limitations. The most potent is levodopa administered with a peripheral decarboxylase inhibitor. However, because its effectiveness declines after long-term use and side effects increase in severity, it should be reserved for individuals with established symptoms which are functionally impairing. In patients with minimal symptoms, anticholinergic agents, or agents which facilitate dopaminergic mechanisms normally operative in the nervous system, should be used. In a limited trial, deprenyl has produced promising results during this phase of parkinsonism. Deprenyl's major usefulness however, has been demonstrated in patients under treatment with levodopa which has become complicated by fluctuating responses--particularly those of the end-start-dose variety. In such patients, it is possible to achieve an increase in "on" time and a decrease in the severity of parkinsonism. In most patients, such a response can maintained for a period of two years or longer.

Organic mental syndrome and confusional states in Parkinson's disease. Relationship to computerized tomographic signs of cerebral atrophy.

Ninety-three patients with a diagnosis of Parkinson's disease, otherwise unselected, were specifically evaluated for organic mental syndrome (OMS) and other neurologic motor signs other than those referrable to extrapyramidal dysfunction; in addition, they had cranial computerized tomography (CT) to measure any structural changes in brain parenchyma. Cortical (sulci) atrophy and ventricular enlargement as CT signs of cerebral atrophy were correlated with different clinical patterns of the disease. An age-adjusted control population, with intact mentation, was similarly studied. The presence of classic OMS in a sizable segment of the usual parkinsonian population was invariably associated with CT signs of cerebral atrophy. Atrophic changes on CT scans, however, were not necessarily correlated with any intellectual dysfunction, or only weakly so, independent of age. The "typical" parkinsonian patients without evidence of OMS were indistinguishable from an age-adjusted control group with regard to structural changes in their scans. However, the parkinsonian patients with definite, permanent OMS and other focal neurologic deficit probably constitute a separate or distinct subset of the parkinsonian population, with a pathologic substrate more likely to be similar to that of the so-called Alzheimer-type dementias. Duration of the parkinsonian syndrome was not predictive of either mental status or scan findings, after adjustment for age as a factor.