229 research outputs found

    Cabbage Diseases

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    Cabbage diseases are the chief limiting factor In profitable commerclal cabbage growing In Iowa. The most destructive of these are black·leg, black-rot, and cabbage yellows. Any one may destroy the greater portion of a crop. The first two are known to be distributed with the seed and cause Infection of the young plants In the seed bed. Some of these naturally find their way Into the field and under favorable conditions become destructive. Cabbage yellows may also be distributed with the seed but Is probably more commonly spread with the plants by the soil adhering to the roots

    Diseases of Cucumbers and Melons in Iowa

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    The profitable production of cucumbers, cantaloupes and watermelons, collectively known as cucurblts, depends on the selection of varieties, proper soil conditions, fertilizers, and the control of Insects and diseases. Growers generally realize the Importance of the first three, but neglect the diseases because they do not understand them. Diseases of cucurblts (cucumbers and melons) In Iowa have become so serious that these crops have been discontinued by many growers even where soil and other conditions are very favorable. The diseases affecting cucumbers and melons are caused In some cases by bacteria, In others by fungi and one Is due to a virus. These organisms live In the cucumber and melon plants, and require right conditions for good growth. Cool, damp weather Is most favorable for the growth and development of fungi and bacteria. Under such conditions the crop losses Incurred are largely due to the Increased activities of these organisms.</p

    Pythium Graminicola Subr. on Barley

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    Pythium graminicola was constantly isolated from infected roots of barley grown on the experimental plots of the Northern Iowa Agricultural Experimental Farm, Kanawha, and from plants grown on the plots at the Agronomy Farm at Ames, Iowa, in 1936 to 1939, inclusive. The symptoms of Pythium graminicola on barley were: Seed decay, seedling blight, root necrosis, yellowing and curling of leaves and stunting. Pythium root necrosis was very severe in 1936 and in 1938. The injury to the seedlings was greater at high temperature than at low. The pathogen grew very slowly at 15° c., which may in part explain the larger yields incident to early seedings

    A study of Sclerospora Graminicola (Sacc.) Schroet. on Setaria Viridis (L.) Beauv. and Zea Mays L.

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    Conidial sporulation of Sclerospora graminicola has been observed in the day time occurring naturally in the field and under artificial conditions in the laboratory. The period required for the development of mature conidia lies between 4 hours 35 minutes and 111/2 hours. The conditions which seem necessary for the production of conidia, whether during the day or night, are: a completely saturated atmosphere, turgid host leaves, a slight moisture film on the surface of the leaves and a temperature ranging between 8° and 27 °C. When flooded into a drop of water immediately after being discharged, conidia were found to germinate after 60 minutes. The best germination was obtained at 15°C., but the optimum was not definitely determined. Normal conidia measure 14-23 x 11-17µ. Sometimes larger conidia are produced (43 x 18.6µ) . The average length of conidiophores of Sclerospora graminicola was found to be 267.8µ while the individuals measured ranged from 214.5 to 375.3µ, a variation of 160.8µ. Spores were found to be forcefully discharged from the conidiophores thru a distance of 2.5 mm. vertically and 1.89 mm. horizontally. Setaria viridis, S. italica, Zea mays (May\u27s Golden popcorn) and Euchlaena mexicana were infected with Sclerospora graminicola when exposed to the conidia of the mildew. Oospores of Sclerospora graminicola were found to overwinter naturally in field soil under Iowa conditions. In one test, oospores which overwintered outdoors gave nearly twice as much infection on Setaria viridis and Zea Mays (Japanese Hulless popcorn) as did the oospores which were kept in the laboratory, Plants from five genera of Gramineae were found to be susceptible hosts to Sclerospora graminicola. These are: Euchlaena, Setaria, Holcus, Saccharum and Zea. Setaria viridis was found to be the most susceptible of all hosts and popcorn more susceptible than sweet corn and dent corn. Six days were found to be the usual period of incubation between the time oospores were placed on the seeds and that when conidial fruiting appeared on the leaves. Infection by oospores was obtained from the time the testa was broken until the emergence of the plumule above ground. Relative susceptibility of seedlings decreases with age. The processes connected with infection are more greatly favored by temperatures of 15° to 16°C. than by temperatures of 24° to 30°C. The germinating oospore is evidently unable to penetrate older leaf tissue. The viability of oospores was little affected by soaking in 2 percent copper sulfate solutions for 10 minutes, while similar treatment in 1 percent formaldehyde for 5 minutes proved fatal. The killing action of mercuric chloride 1-1000 was not so great as that of formaldehyde. Freshly collected oospores which were held in a dry condition at 77°C. for 1 hour later gave 52 percent infection on Setaria viridis, while wet spores lost their viability to a marked degree when held at 50°C. for a similar period. Sclerospora graminicola was studied in the field during the summers of 1925, 1926 and 1927. Infection was obtained on corn and teosinte planted in plots which had been artificially infested with oospores. Spontaneous conidial sporulation was found to be comparatively rare on corn in the field altho it was observed in 1926 and 1927 on young seedlings during periods of high humidity and cool temperatures. Infected plants were either killed outright or became stunted and unproductive. A few plants apparently outgrew the attack. In Iowa, Sclerospora graminicola has been observed only twice occurring naturally on corn in the field. Oospores of Sclerospora graminicola which had been held 30 months under dry conditions in the laboratory were found to be viable. Presoaking of oospores does not seem to affect the percentage of infection. Soil is not necessary as a medium for the germination of oospores

    Obesity measures, metabolic health and their association with 15-year all-cause and cardiovascular mortality in the SAMINOR 1 Survey:a population-based cohort study

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    Background - The mortality of metabolic-obesity phenotypes has been thoroughly studied, but it is not known if or how the association between mortality and body mass index (BMI), waist circumference or a body shape index (ABSI) differ in strata of cardiometabolic health status. Methods - We linked data on 12,815 men and women aged 36–79 years from the SAMINOR 1 Survey with mortality data from the Norwegian Cause of Death Registry. We defined metabolically healthy and unhealthy as having zero and ≥ 1, respectively, of the following: MetS, pre-existing diabetes or cardiovascular disease (CVD), or prescribed drugs for high blood pressure, hyperglycaemia or dyslipidaemia. We defined general and abdominal obesity as BMI ≥ 30 kg/m2 and waist circumference ≥ 88 cm (women) or 102 cm (men), respectively, and cross-classified these categories with metabolic status to create metabolically healthy non-obese and obese (MHNO and MHO) and metabolically unhealthy non-obese and obese (MUNO and MUO) phenotypes. We used Cox regression to estimate the hazard ratio (HR) for all-cause and CVD mortality for 1) the four phenotypes and 2) BMI, waist circumference and ABSI fitted with restricted cubic splines. We adjusted for age and lifestyle, and tested for interactions with sex and metabolic status (only continuous measures). Results - The MHO phenotype was present in 7.8% of women and 5.8% of men. During a median follow-up of 15.3/15.2 years, 596/938 women/men had died, respectively. The MUNO and MUO groups had higher mortality than the MHNO group. Sex and phenotypes interacted with respect to CVD mortality: relative to the MHNO group, the MHO group had an adjusted HR (95% confidence interval) for CVD mortality of 1.05 (0.38–2.88) in women and 2.92 (1.71–5.01) in men. We found curvilinear associations between BMI/waist circumference and all-cause mortality irrespective of metabolic status. Corresponding relationships with CVD mortality were linear and the slope differed by sex and metabolic status. ABSI was linearly and positively associated with all-cause and CVD mortality in men. Conclusion - The relationships between BMI, waist circumference or ABSI and mortality differed by sex, metabolic status and cause of death. Poor metabolic health substantially increases mortality regardless of obesity status

    Gene Expression and Distribution of Key Bone Turnover Markers in the Callus of Estrogen-Deficient, Vitamin D-Depleted Rats

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    An experimental rat model was used to test the hypothesis that in osteoporosis (OP) the molecular composition of the extracellular matrix in the fracture callus is disturbed. OP was induced at 10 weeks of age by ovariectomy and a vitamin D3-deficient diet, and sham-operated animals fed normal diet served as controls. Three months later a closed tibial fracture was made and stabilized with an intramedullary nail. After 3 and 6 weeks of healing, the animals were killed and the fracture calluses examined with global gene expression, in situ mRNA expression, and ultrastructural protein distribution of four bone turnover markers: osteopontin, bone sialoprotein, tartrate-resistant acid phosphatase, and cathepsin K. Global gene expression showed a relatively small number of differently regulated genes, mostly upregulated and at 3 weeks. The four chosen markers were not differently regulated, and only minor differences in the in situ mRNA expression and ultrastructural protein distribution were detected. Gene expression and composition of fracture calluses are not generally disturbed in experimental OP

    Retinoic Acid Increases Proliferation of Human Osteoclast Progenitors and Inhibits RANKL-Stimulated Osteoclast Differentiation by Suppressing RANK

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    It has been shown that high vitamin A intake is associated with bone fragility and fractures in both animals and humans. However, the mechanism by which vitamin A affects bones is unclear. In the present study, the direct effects of retinoic acid (RA) on human and murine osteoclastogenesis were evaluated using cultured peripheral blood CD14+ monocytes and RAW264.7 cells. Both the activity of the osteoclast marker tartrate resistant acid phosphatase (TRAP) in culture supernatant and the expression of the genes involved in osteoclast differentiation together with bone resorption were measured. To our knowledge, this is the first time that the effects of RA on human osteoclast progenitors and mature osteoclasts have been studied in vitro. RA stimulated proliferation of osteoclast progenitors both from humans and mice. In contrast, RA inhibited differentiation of the receptor activator of nuclear factor κB ligand (RANKL)-induced osteoclastogenesis of human and murine osteoclast progenitors via retinoic acid receptors (RARs). We also show that the mRNA levels of receptor activator of nuclear factor κB (RANK), the key initiating factor and osteoclast associated receptor for RANKL, were potently suppressed by RA in osteoclast progenitors. More importantly, RA abolished the RANK protein in osteoclast progenitors. This inhibition could be partially reversed by a RAR pan-antagonist. Furthermore, RA treatment suppressed the expression of the transcription factor nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) and increased the expression of interferon regulatory factor-8 (IRF-8) in osteoclast progenitors via RARs. Also, RA demonstrated differential effects depending on the material supporting the cell culture. RA did not affect TRAP activity in the culture supernatant in the bone slice culture system, but inhibited the release of TRAP activity if cells were cultured on plastic. In conclusion, our results suggest that retinoic acid increases proliferation of human osteoclast progenitors and that it inhibits RANK-stimulated osteoclast differentiation by suppressing RANK

    Itch and skin rash from chocolate during fluoxetine and sertraline treatment: Case report

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    BACKGROUND: The skin contains a system for producing serotonin as well as serotonin receptors. Serotonin can also cause pruritus when injected into the skin. SSRI-drugs increase serotonin concentrations and are known to have pruritus and other dermal side effects. CASE PRESENTATION: A 46-year-old man consulted his doctor due to symptoms of depression. He did not suffer from any allergy but drinking red wine caused vasomotor rhinitis. Antidepressive treatment with fluoxetine 20 mg daily was initiated which was successful. After three weeks of treatment an itching rash appeared. An adverse drug reaction (ADR) induced by fluoxetine was suspected and fluoxetine treatment was discontinued. The symptoms disappeared with clemastine and betametasone treatment. Since the depressive symptoms returned sertraline medication was initiated. After approximately two weeks of sertraline treatment he noted an intense itching sensation in his scalp after eating a piece of chocolate cake. The itch spread to the arms, abdomen and legs and the patient treated himself with clemastine and the itch disappeared. He now realised that he had eaten a chocolate cake before this episode and remembered that before the first episode he had had a chocolate mousse dessert. He had never had any reaction from eating chocolate before and therefore reported this observation to his doctor. CONCLUSIONS: This case report suggests that there may be individuals that are very sensitive to increases in serotonin concentrations. Dermal side reactions to SSRI-drugs in these patients may be due to high activity in the serotonergic system at the dermal and epidermo-dermal junctional area rather than a hypersensitivity to the drug molecule itself

    Risk factors for and preventability of drug‐related hospital revisits in older patients: A post‐hoc analysis of a randomized clinical trial

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    Aim: The aims of this study were (1) to identify older patients' risk factors for drug-related readmissions and (2) to assess the preventability of older patients' drug-related revisits. Methods: Post hoc analysis of a randomized clinical trial with patients aged ≥65 years at eight wards within four hospitals in Sweden. (1) The primary outcome was risk factors for drug-related readmission within 12 months post-discharge. A Cox proportional hazards model was made with sociodemographic and clinical baseline characteristics. (2) Four hundred trial participants were randomly selected and their revisits (admissions and emergency department visits) were assessed to identify potentially preventable drug-related revisits, related diseases and causes. Results: (1) Among 2637 patients (median age 81 years), 582 (22%) experienced a drug-related readmission within 12 months. Sixteen risk factors (hazard ratio >1, P < 0.05) related to age, previous hospital visits, medication use, multimorbidity and cardiovascular, liver, lung and peptic ulcer disease were identified. (2) The 400 patients experienced a total of 522 hospital revisits, of which 85 (16%) were potentially preventable drug-related revisits. The two most prevalent related diseases were heart failure (n = 24, 28%) and chronic obstructive pulmonary disease (n = 13, 15%). The two most prevalent causes were inadequate treatment (n = 23, 27%) and insufficient or no follow-up (n = 22, 26%). Conclusion: (1) Risk factors for drug-related readmissions in older hospitalized patients were age, previous hospital visits, medication use and multiple diseases. (2) Potentially preventable drug-related hospital revisits are common and might be prevented through adequate pharmacotherapy and continuity of care in older patients with cardiovascular or lung disease
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