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What kind of ribes is this?

What kind of ribes is this?



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I have a plant in my USDA zone 5 garden that appears to be in the ribes genus.

Details:

  • The location is east of Toronto (Ontario, Canada).
  • The plant is currently flowering (today is May 18th, 2019).
  • It is approx 4 feet tall.
  • The plant flowers every year, but does not set fruit (not self-fruitful).

More photos here:

  1. https://i.stack.imgur.com/coEp5.jpg">https://i.stack.imgur.com/wv0TA.jpg">https://i.stack.imgur.com/pFmtk.jpg">https://i.stack.imgur.com/KvjGe.jpg">

    I think this is Ribes americanum or wild black currant.

    I'm basing this on page 306 of Newcomb's Wildflower Guide, an excellent source for the Eastern US and some of Canada. On that page we have two main choices:

    1. Base of flowers prickly or bristly… or

    2. Base of flowers not prickly or bristly…

    Your excellent pictures suggest that your specimen is in category 2.

    From there, we have:

    a. Flowers solitary or 2-3 in a cluster; branches bearing a few thorns. or

    b. Flowers 5 or more in racemes.

    Your specimen looks to have quite a few flowers, so in category 2b we have a choice of Ribes americanum:

    Whitish or yellowish flowers, longer than wide (and fruit black, you can check later I guess),

    or Ribes sativum:

    Greenish flowers, wider than long (and fruit red).

    Color in the white/green/yellow range is a bit subjective, but your flowers look longer than wide, hence Ribes americanum.

    Of course, with this in mind you might re-inspect the plant and refine this a bit.


    Rubus

    Raspberries, blackberries, and dewberries are common, widely distributed members of the genus. Most of these plants have woody stems with prickles like roses spines, bristles, and gland-tipped hairs are also common in the genus. The Rubus fruit, sometimes called a bramble fruit, is an aggregate of drupelets. The term "cane fruit" (or "cane-fruit"), or "cane berry" (or "caneberry"), applies to any Rubus species or hybrid which is commonly grown with supports such as wires or canes, including raspberries, blackberries, and hybrids such as loganberry, boysenberry, marionberry and tayberry. [5] The stems of such plants are also referred to as canes.


    Rib Structure

    There are two classifications of ribs – atypical and typical. The typical ribs have a generalised structure, while the atypical ribs have variations on this structure.

    Typical Ribs

    The typical rib consists of a head, neck and body:

    The head is wedge shaped, and has two articular facets separated by a wedge of bone. One facet articulates with the numerically corresponding vertebrae, and the other articulates with the vertebrae above.

    The neck contains no bony prominences, but simply connects the head with the body. Where the neck meets the body there is a roughed tubercle, with a facet for articulation with the transverse process of the corresponding vertebrae.

    The body, or shaft of the rib is flat and curved. The internal surface of the shaft has a groove for the neurovascular supply of the thorax, protecting the vessels and nerves from damage.

    Fig 2 – The bony landmarks of a typical rib.

    Atypical Ribs

    Ribs 1, 2, 10 11 and 12 can be described as ‘atypical’ – they have features that are not common to all the ribs.

    Rib 1 is shorter and wider than the other ribs. It only has one facet on its head for articulation with its corresponding vertebrae (there isn’t a thoracic vertebra above it). The superior surface is marked by two grooves, which make way for the subclavian vessels.

    Rib 2 is thinner and longer than rib 1, and has two articular facets on the head as normal. It has a roughened area on its upper surface, from which the serratus anterior muscle originates.

    Rib 10 only has one facet – for articulation with its numerically corresponding vertebrae.

    Ribs 11 and 12 have no neck, and only contain one facet, which is for articulation with their corresponding vertebrae.


    Analysis, Identification, and Quantification of Anthocyanins in Fruit Juices

    Tânia G. Albuquerque , . Helena S. Costa , in Fruit Juices , 2018

    34.5.11 Redcurrant

    Redcurrant or red currant belongs to genus Ribes from gooseberry family and is native from Western Europe, but nowadays it is widely spread worldwide. If consumed regularly, redcurrants have been related with a decrease in the incidence of many chronic diseases, namely cardiovascular diseases, diabetes, and cancer ( Zdunić et al., 2016 ). In the literature, a comparative analysis of anthocyanin content among different varieties of redcurrants (Ribes rubrum L.) have been performed, and considerable differences were found especially regarding the amounts ( Stój et al., 2006 ). However, concerning the anthocyanin profile, for all the selected varieties of redcurrant juices, the most abundant anthocyanin was cyanidin-3-rutinoside, with amounts that varied between 27.4 and 77 mg/100 mL ( Stój et al., 2006 ).


    Control of Plant Virus Diseases

    Robert R. Martin , Ioannis E. Tzanetakis , in Advances in Virus Research , 2015

    1 Introduction

    The term berry (small fruit) refers primarily to the genera Fragaria (strawberry), Rubus (blackberry, raspberry, and their hybrids), Vaccinium (blueberry and cranberry), Ribes (currants and gooseberry), and Sambucus (elderberry). Traditionally, berry crops have been collected from the wild at the dawn of the human species and only recently they have become agricultural crops, especially after the development of the modern strawberry (F. x ananassa). In a short period of time and because of their ever growing popularity with consumers, berry crops have been developed to grow across the globe from subtropical to subarctic environments. The major expansion in production and the environments where these crops are grown, along with the rapid changes in the genotypes grown commercially, have resulted in a very diverse virosome in berry crops ( Martin, MacFarlane, et al., 2013 Martin, Peres, & Whidden, 2013 Martin, Polashock, & Tzanetakis, 2012 Martin & Tzanetakis, 2006 ). Those changes and the development of new technologies allowing for the rapid discovery of new viruses have led to a substantial increase in the number of known berry viruses, which has more than doubled in the last 20 years. The number of new discoveries still increases with more than eight berry viruses identified in each of the last 3 years ( Martin et al., 2012 Martin, MacFarlane, et al., 2013 Martin, Peres, et al., 2013 Martin et al., unpublished Tzanetakis et al., unpublished). This communication aims to provide a general overview of how basic knowledge on berry viruses can be used for efficient virus control during the propagation process and field establishment.

    There are more than 80 species in 30 virus genera known to infect the major berry crops (here we will only present the ones communicated in peer-reviewed publications as of May 2014). Most viruses identified before the 1990s are well-studied at the molecular and biological level, whereas, newly identified viruses are characterized primarily at the molecular level. This has led to knowledge gaps that need to be addressed. For the purpose of this communication, we will provide control strategies for those less-studied viruses based on their taxonomic placement and the accumulated biological knowledge on closely related viruses. Based on molecular data, the best guesses of potential vectors need to be considered, ranging from whiteflies to eriophyid mites to fungi. The number of vector taxa in a particular area may be such that control of all vectors is unfeasible. In general terms, areas with tradition of berry production have a set group of viruses of concern. In most cases, there is the know-how on viruses/vectors and their control, whereas new production areas tend to have a wider array of viruses, many of which have only recently been discovered. A list of viruses infecting each of the major berry crops, their mode of transmission and their geographic range (where known) are presented in individual tables. Aphids are major virus vectors for all berries crops. They are abundant at the traditional production areas in the temperate regions around the world and just a few years ago they were considered the only vector of concern for most production areas. In most crops, the prominent aphid species colonizing the crop are also the major vectors, able to transmit an array of viruses that tend to act synergistically to cause disease as in the case of strawberry decline or raspberry mosaic ( Martin & Tzanetakis, 2006 Quito-Avila, Lightle, & Martin, 2014 ). Notwithstanding, there are opportunistic feeders that may transmit without colonizing plants (Myzus ornatus Lowery, Bernardy, Deyoung, & French, 2008 ). When an aphid species is crop-specific, control can be achieved through chemical sprays or even more efficiently, in the case of strawberry with crop-free times, an applicable practice for nurseries that are not neighboring commercial fields.

    Nematode-transmitted viruses can cause significant losses and even plant death ( Martin, MacFarlane, et al., 2013 Martin, Peres, et al., 2013 Martin et al., 2012 Martin & Tzanetakis, 2006 ). The major viruses infecting berry crops belong to the genus Nepovirus and the unassigned Strawberry latent ringspot virus. One of the major caveats with members of this group is their wide host range that extends to several common weeds present in berry fields. As nematode movement is restricted to less than 2 m/year, they have been successfully controlled with the use of potent nematicides such as methyl bromide. With the phase-out of the more efficient nematicides, this virus group may reemerge especially, in areas where the nematode vectors are endemic.

    Pollen and seed-transmitted viruses (PSTVs) present the most challenging group when it comes to control because the only viable control method is avoidance. In many cases, PSTVs cause significant losses in single or mixed infections whereas several of them infect multiple berry crops ( MacDonald, Martin, & Bristow, 1991 Martin, MacFarlane, et al., 2013 Martin, Peres, et al., 2013 Pallas et al., 2012 ). Some of the PSTVs do not have an active vector and can move passively by wind currents and pollinating arthropods such as bees, thrips ( Sdoodee & Teakle, 1987 ), and mites, whereas others may have insect or nematode vectors, in which case control of their primary vectors can significantly reduce spread.

    Whiteflies have only been identified recently as virus vectors in berry crops although there have been diseases, first reported in the 1950s, that have now been proven to be caused by whitefly-transmitted viruses ( Tzanetakis et al., 2004 Tzanetakis, Wintermantel, & Martin, 2003 ). The emergence of this virus group as a major limiting factor to production is primarily due to the expansion of berry production to the subtropics and the extension of the geographic range of whiteflies to the temperate regions around the world. Notwithstanding, the number of whitefly-transmitted viruses is still limited and only includes species that infect strawberry and blackberry. In all cases, those viruses do not cause high-impact symptoms in single infections but act synergistically with other viruses in mixed infections to cause detrimental symptoms that can even lead to plant death ( Martin & Tzanetakis, 2013 Susaimuthu, Tzanetakis, Gergerich, Kim, & Martin, 2008 Susaimuthu, Tzanetakis, Gergerich, & Martin, 2008 ). This should be a concern for certification programs and for nursery systems where quite often disease evaluation is based on visual observations. With many viruses of the berry crops, plants infected with one or two viruses may be asymptomatic in nursery plants and pass visual inspections, but when moved to production fields and infected with additional viruses they can decline rapidly ( Martin & Tzanetakis, 2013 ).

    Virus-vectoring eriophyid mites were discovered recently in berry crops although some of the diseases they are associated with have been reported since the beginning of the twentieth century ( Jones, Gordon, & Jennings, 1984 ). The lack of knowledge on the biology of these vectors and the absence of systemic miticides make vector control challenging. To date, most berry mite-transmitted viruses belong to the genus Emaravirus ( Hassan, Keller, Martin, Sabanadzovic, & Tzanetakis, 2013 McGavin, Mitchell, Cock, Wright, & MacFarlane, 2012 ), viruses that appear to be localized at the mite feeding sites, but there are indications that several new berry-infecting systemic RNA viruses are also mite-transmitted and involved in important diseases, primarily as part of virus complexes ( Sabanadzovic, Abou Ghanem-Sabanadzovic, & Tzanetakis, 2011 ). A major exception is Black currant reversion virus (BRV), which taxonomically belongs to the genus Nepovirus but is transmitted by the black currant gall mite ( Susi, 2004 ). BRV exemplifies the need for experimental verification of a virus vector as predictions based on molecular data and taxonomy may be deceiving.

    Leafhoppers are another group recently identified as potential virus vectors for berry crops. To date, there are at least four blackberry viruses in the genus Marafivirus ( Sabanadzovic & Abou Ghanem-Sabanadzovic, 2009 Sabanadzovic, Ghanem-Sabanadzovic, & Gorbalenya, 2009 Sabanadzovic et al., unpublished), and other viruses in this genus are known to be transmitted by leafhoppers. A study in the southeastern United States identified about 50 leafhopper species in production fields (Johnson et al., unpublished), indicative of the complex virus/vector interactions that need to be elucidated before the development of meaningful control strategies.

    The only thrips-transmitted virus known to infect berry crops is Impatiens necrotic spot virus (INSV), detected in blackberry ( Tzanetakis, Guzmán-Baeny, VanEsbroeck, Fernandez, & Μartin, 2009 ). There is no detailed work performed on transmission of the virus in blackberry that would elucidate the efficiency of transmission or the thrips species that are the primary vectors of the virus in blackberry. However, the excessive number of thrips found in several fields and the low numbers of INSV-infected plants indicate rather inefficient transmission probably because of the thrips composition in blackberry fields, or the presence of diverse flora in many blackberry fields in the southeastern United States.

    A new insect group was recently added in the list of berry virus vectors. After the discovery of Blackberry vein banding associated virus (BVBaV Thekke-Veetil et al., 2013 ), a member of the genus Ampelovirus, experiments were performed with mealybugs that colonize plants and successfully demonstrated transmission (Sabanadzovic et al., unpublished). As is the case with several of the berry viruses, BVBaV does not appear to cause symptoms in single infections but is often found in mixed virus infections in declining plants.

    The last virus group with a single representative in the list of berry viruses to date is that transmitted by fungi. Blueberry mosaic is a disease that was first described about 60 years ago and only recently was a virus associated with the disease, Blueberry mosaic associated virus (BlMaV). BlMaV belongs to the genus Ophiovirus and has been detected in all plants with typical disease symptoms ( Thekke-Veetil, Ho, Keller, Martin, & Tzanetakis, 2014 ). Transmission experiments are underway, and the virus is hypothesized to be transmitted by members of the genus Olpidium, as is the case with other members of the genus.


    Contents

    Verticillium spp. attack a very large host range including more than 350 species of vegetables, fruit trees, flowers, field crops, and shade or forest trees. Most vegetable species have some susceptibility, so it has a very wide host range. [1] A list of known hosts is at the bottom of this page.

    The signs are similar to most wilts with a few specifics to Verticillium. Wilt itself is the most common sign, with wilting of the stem and leaves occurring due to the blockage of the xylem vascular tissues and therefore reduced water and nutrient flow. In small plants and seedlings, Verticillium can quickly kill the plant while in larger, more developed plants the severity can vary. Some times only one side of the plant will appear infected because once in the vascular tissues, the disease migrates mostly upward and not as much radially in the stem. [2] Other symptoms include stunting, chlorosis or yellowing of the leaves, necrosis or tissue death, and defoliation. Internal vascular tissue discoloration might be visible when the stem is cut. [1]

    In Verticillium, the signs and effects will often only be on the lower or outer parts of plants or will be localized to only a few branches of a tree. In older plants, the infection can cause death, but often, especially with trees, the plant will be able to recover, or at least continue living with the infection. The severity of the infection plays a large role in how severe the signs are and how quickly they develop. [1]

    While Verticillium spp. are very diverse, the basic life cycle of the pathogen is similar across species, except in their survival structures. The survival structures vary by species with V. albo-atrum forming mycelium, V. dahliae forming microsclerotia, V. nigrescens and V. nubilum forming chlamydospores, and V. tricorpus forming all three. While resting, many factors such as soil chemistry, temperature, hydration, micro fauna, and non-host crops all have an effect on the viability of the resting structure. Mycelium have been observed remaining viable for at least 4 years, [3] while microsclerotia have been observed in fields planted with non-host crops for over 10 years [4] and even 15 years has been reported. [1] Viability is reduced at these extremes, but the long survivability of these structures is an important aspect for Verticillium control.

    When roots of a host crop come near the resting structure (about 2mm), [5] root exudate promotes germination and the fungi grows out of the structure and toward the plant. Being a vascular wilt, it will try to get to the vascular system on the inside of the plant, and therefore must enter the plant. Natural root wounds are the easiest way to enter, and these wounds occur naturally, even in healthy plants because of soil abrasion on roots. Verticillium has also been observed entering roots directly, but these infections rarely make it to the vascular system, especially those that enter through root hairs. [6]

    Once the pathogen enters the host, it makes its way to the vascular system, and specifically the xylem. The fungi can spread as hyphae through the plant, but can also spread as spores. Verticillium produce conidia on conidiophores and once conidia are released in the xylem, they can quickly colonize the plant. Conidia have been observed traveling to the top of cotton plants, 115 cm, 24 hours after initial conidia inoculation, so the spread throughout the plant can occur very quickly. [7] Sometimes the flow of conidia will be stopped by cross sections of the xylem, and here the conidia will spawn, and the fungal hyphae can overcome the barrier, and then produce more conidia on the other side. [8]

    A heavily infected plant can succumb to the disease and die. As this occurs, the Verticillium will form its survival structures and when the plant dies, its survival structures will be where the plant falls, releasing inoculates into the environment. The survival structures will then wait for a host plant to grow nearby and will start the cycle all over again.

    Besides being long lasting in the soil, Verticillium can spread in many ways. The most common way of spreading short distances is through root to root contact within the soil. Roots in natural conditions often have small damages or openings in them that are easily colonized by Verticillium from an infected root nearby. Air borne conidia have been detected and some colonies observed, but mostly the conidia have difficulty developing above ground on healthy plants. [9] In open channel irrigation, V. dahliae have been found in the irrigation ditches up to a mile from the infected crop.

    Without fungicidal seed treatments, infected seeds are easily transported and the disease spread, and Verticillium has been observed remaining viable for at least 13 months on some seeds. Planting infected seed potatoes can also be a source of inoculum to a new field. Finally, insects have also been shown to transmit the disease. Many insects including potato leaf hopper, leaf cutter bees, and aphids have been observed transmitting conidia of Verticillium and because these insects can cause damage to the plant creating an entry for the Verticillium, they can help transmit the disease. [2]

    While Verticillium wilts often have the same symptoms of Fusarium wilts, Verticillium can survive cold weather and winters much better than Fusarium, which prefers warmer climates. The resting structures of Verticillium are able to survive freezing, thawing, heat shock, dehydration, and many other factors and are quite robust and difficult to get rid of. The one factor they do not tolerate well is extended periods of anaerobic conditions (such as during flooding). [2]

    Verticillium will grow best between 20 and 28 degrees Celsius, [1] but germination and growth can occur well below (or above) those temperatures. Water is necessary for resting structure germination, but is not as important for the spread of the fungus as in many other fungi. While not an environmental requirement for the fungus, stressed plants, often brought on by environmental changes, are easier to attack than healthy plants, so any conditions that will stress the plant but not directly harm the Verticillium will be beneficial for Verticillium wilt development. [2]

    Verticillium wilt begins as a mild, local infection, which over a few years will grow in strength as more virile strains of the fungus develop. If left unchecked the disease will become so widespread that the crop will need to be replaced with resistant varieties, or a new crop will need to be planted altogether. [1]

    Control of Verticillium can be achieved by planting disease–free plants in uncontaminated soil, planting resistant varieties, and refraining from planting susceptible crops in areas that have been used repeatedly for solanaceous crops. Soil fumigation can also be used, with chloropicrin being particularly effective in reducing disease incidence in contaminated fields.

    In tomato plants, the presence of ethylene during the initial stages of infection inhibits disease development, while in later stages of disease development the same hormone will cause greater wilt. Tomato plants are available that have been engineered with resistant genes that will tolerate the fungus while showing significantly lower signs of wilting. [1]

    Verticillium albo-altrum, Verticilium dahliae and V. longisporum can overwinter as melanized mycelium or microsclerotia within live vegetation or plant debris. As a result, it can be important to clear plant debris to lower the spread of disease. Verticilium dahliae and V. longisporum are able to survive as microsclerotia in soil for up to 15 years. [1]

    Verticillium wilt occurs in a broad range of hosts but has similar devastating effects on many of these plants. In general, it reduces the quality and quantity of a crop by causing discoloration in tissues, stunting, and premature defoliation and death. [10] Stock from infested nurseries may be restricted. Once a plant is infected, there is no way to cure it. Verticillium wilt is especially a concern in temperate areas and areas that are irrigated. Verticllium spp. can naturally occur in forest soils and when these soils are cultivated, the pathogen will infect the crop. [1]

    The Salinas Valley in California has had severe problems with Verticillium wilt since 1995, most likely due to flooding in the winter of 1995. Many areas in the Salinas and Pajaro Valleys are unable to grow lettuce due to the high levels of Verticillium dahliae in the soil. [11] Potatoes grown in Verticillium infested soils may have a reduced yield between 30–50% compared to potatoes grown in "clean" soil. Verticillium wilt has also caused a shift in peppermint cultivation from the Midwest in the mid- to late-1800s to western states such as Oregon, Washington and Idaho, to new, non-infested areas within these states now. [10]

    Replanting susceptible species on the site of a removed plant that has succumbed to V. albo-atrum or V. dahliae is inadvisable because of the heightened risk of infection. Instead, resistant or immune varieties should be used. The following two lists show both susceptible and resistant/immune plants by Latin name. [12] [13] [14] [15] [16] [17]

    (*) indicates that the plant occurs on both lists because different varieties or cultivars vary in their resistance.
    (#) indicates that some strains are resistant.
    (+) indicates susceptibility to some European strains of Verticillium albo-atrum.


    Academic Hood Colors List

    This Academic Hood Colors List serves an important function for your set of graduation Academic Regalia (hood, tam, and gown). The regalia hood colors typically include four sections: shell fabric, velvet edge, satin field, and satin chevron. The color of the velvet edge is determined using this official degree color chart. That velvet edge hood color, sometimes known as Academic Regalia Inter-Collegiate Colors, represents your specific degree or discipline. The satin field and chevron (the hood lining colors) represent your university or college school colors. The overall size and shape represents the type of degree: bachelor's, master's, or doctoral (with the narrow end getting progressively longer with the higher ranking degrees). Finally, the fabric shell color simply matches the fabric color of the graduation gown, which is usually black but sometimes is another color depending on the degree-granting institution. Associate degrees use a special cowl instead of a hood.

    Below is the official academic regalia hood color list. Your academic hood colors are ultimately the decision of your degree-granting institution and you. However, these are the official academic regalia colors.

    See the footnote for PhD degrees, rules regarding multiple degrees, and determining your field and chevron colors.

    Academic Regalia Inter-Collegiate Colors


    Drab Maize Blue-Violet White Light Blue
    Accounting Agriculture Architecture Arts Arts in Education
    Drab Drab Scarlet Nile Green Silver
    Business Administration Business Education Canon Law Chiropody Chiropractic
    Blue-Violet Orange Drab Drab Crimson
    City Planning Civil Engineering Commerce Commercial Science Communication
    Russet Light Blue Science Gold Midnight Blue Lilac
    Conservation Counseling and Guidance Criminology Criminal Justice Dental Surgery
    Lilac Scarlet Brown Copper Light Blue
    Dentistry Divinity Dramatic Arts Economics Education
    Orange White Science Gold Brown Aquamarine
    Engineering English Environmental Science Fine Arts Foreign Affairs
    Peacock Blue Russet Peacock Blue Sage Green White
    Foreign Service Forestry Government Health and Rehabilitation History
    Sage Green Science Gold Drab Bilberry Crimson
    Hygiene Industrial Arts Industrial and Labor Relations Interior Design Journalism
    Purple Purple White White Lemon
    Jurisprudence Law Letters Literature Library Science
    Science Gold Kelly Green Science Gold Pink Silver
    Mathematics Medicine Military Science Music Naprapathy
    Apricot Aquamarine Silver Kelly Green Light Blue
    Nursing Optometry Oratory Osteopathy Pedagogy
    Peacock Blue Olive Science Gold Dark Blue Sage Green
    Personnel Services Pharmacy Philanthropy Philosophy* Physical Science
    Science Gold Nile Green Science Gold Dark Blue Gold
    Physics Podiatry Police Science Political Science Psychology
    Peacock Blue Salmon Pink Peacock Blue Blue-Violet Light Blue
    Public Administration Public Health Public Service Regional Planning Religious Education
    Scarlet Citron Science Gold Dark Blue Citron
    Sacred Theology Sanitary Science Science Social Ethics Social Science
    Citron Citron White Silver Nile Green
    Social Service Social Work Sociology Speech Surgical Chiropody
    Scarlet Citron Blue-Violet Gray Dark Blue
    Theology Urban Life Urban Planning Veterinary Science PhD Blue *

    * In determining your academic regalia colors, please note the following: All PhD degrees (as opposed to Doctorate degrees) use "PhD Blue", which is dark blue, in the academic colors. For example, a Doctorate in Psychology would include in your academic hood colors the color Gold, however a PhD in Psychology would use dark blue. If you are unsure if your degree is a Doctorate or PhD, please contact your administrative advisor to determine your precise degree title and academic regalia hood colors.

    If you have multiple degrees, the rule is that you use only one hood, and only one degree/discipline color. You use the hood and color that represents your highest ranking degree (with Doctoral as highest, Masters as second highest, Bachelors as third highest, and Associate as the lowest). If you have two different degrees at the same highest ranking degree, you generally use the most recently awarded degree as your hood.

    If you have an unlisted degree, there is no official color and it is dependant on the individual college or university to determine the color to be used for your hood. Typically, the most similar degree on the official chart is chosen. For example, if your degree is in an advance computer science field, usually the school chooses Science Gold for the degree color.

    Hood Lining Colors (Field and Chevron)

    The above list describes only your velvet colors. There are three additional colors that typically go into your hood. They are the shell fabric (usually black, but sometimes the color of your robe if your robe is a special color that your university uses), and the lining colors.

    Hoods are lined with the official color or colors of the college or university conferring the degree. More than one color is shown by division of the field color in a variety of ways. Most schools divide the color by using a single chevron. Occasionally, a school might use more than one chevron, no chevron but instead a single field color, an equal division, a reverse chevron, a straight bar, or other methods. While Academic Apparel can make any variety of hood, please note that the online ordering system assumes a single field and a single standard chevron. For other unusual types of hoods, you will have to use our downloadable fax forms.

    Starlight Washable Satin (for hood school colors - Professional Style Hoods Only)

    Victorian Gold Eggshell Swiss Mocha Cashmere Sage Victorian Mauve Silver Burgundy Black Kelly
    Desert Blue Navy Regal Gold Royal White Red Crepe Purple New Hunter Kelly Acetate* Orange Acetate*

    * Indicates a color not yet available in washable satin. These are instead substituted with acetate satins, which must be dry cleaned.

    Polyester Taffeta (for hood school colors - Verona Style Hoods Only)

    Royal Blue Hunter Green Red White Burgundy Light Blue
    Gold Navy Blue Kelly Green Silver Purple Black

    The official "Academic Costume Code and Academic Ceremony Guide" includes a sentence that reads as follows: "The various academic costume companies maintain complete files on the approved colors for various institutions."

    Once upon a time long ago, that sentence was correct. However, that was before colleges started springing up across the nation at a rapid rate in the last 50 years or so, and before institutions started the practice of changing their hood colors depending on style or taste or the desires of the student body or economics for bulk manufacturing (sometimes even on a yearly basis).

    We are the direct manufacturer of academic regalia. This means one good thing and one bad thing (from your perspective).

    The good thing is our prices are significantly lower than your degree-granting university would charge to sell them to you, yet the quality is the same or better than what they offer. That's because we are a relatively lean organization, independent, with over 60 years of experience, and we do not pay sales representatives, or have retail stores, or have a large advertising and marketing budget.

    The bad thing is we cannot keep up with the changes each university makes to their regalia each year, and therefore require that our customers make their own inquiries to their degree-granting universities to discover what the current regalia colors are supposed to be for that school before placing an order.

    We suggest you find out in advance of ordering what your school colors are, and which goes in the field and which goes in the chevron of the hood. You might also ask the following additional information: 1) whether they use 6 or 8 sides for their tam (if you are buying a tam) 2) whether they use a tam or a mortarboard for a Master's degree (if you are inquiring about a master's gown regalia set) 3) whether they use the standard black for the gown and hood shell color or if they have a special color 4) whether they use an embroidered school emblem or symbol on the gown velvet an dif so what it looks like (these are fairly rare, but a few schools use them) 5) and if there is anything special about the regalia not covered by those questions.

    Generally the best source for this information is the University book store or student store. Someone at most bookstores has all of this information.

    You should know that you have the right to purchase your gown from any manufacturer, and not just the company that has a contract with your university. By getting this information on your own and purchasing your regalia from Academic Apparel, you will be saving money, and getting a regalia set that looks at least as good as what your school offers, and often it looks and feels significantly better than the bulk manufactured chinese gowns many colleges are now selling (and ours will last longer than those gowns too).

    While we would really like to help you obtain this information, and hope to some day send out surveys each year to each university asking for this data, it is beyond our abilities to do so right now. If you are willing to do the footwork to find this information out, we know you will get a superb robe, hood, and tam from us, at prices that cannot be beat.


    Angina pectoris

    Botanical medicines

    Crataegus species (hawthorn): Berry and flowering tops extracts reduce angina attacks, lower blood pressure and serum cholesterol levels improve blood and oxygen supply of heart by dilation of coronary vessels improve metabolic processes in heart improve cardiac energy metabolism, enhancing myocardial function with more-efficient use of oxygen interact with key enzymes to enhance myocardial contractility (Textbook,Crataegus oxyacantha [Hawthorn]”).

    Ammi visnaga (khella): ancient Mediterranean medicinal plant used historically to treat angina and other heart ailments. Constituents dilate coronary arteries mechanism of action similar to calcium channel blocking drugs. Constituent khellin is extremely effective in relieving angina symptoms, improving exercise tolerance, and normalizing ECGs. Higher doses (120 to 150 mg q.d.) of pure khellin are linked to mild side effects (anorexia, nausea, dizziness). Most clinical studies used high doses several studies used only 30 mg khellin q.d., which offered good results with fewer side effects. Khella extracts standardized for khellin content (12%) are preferred at dose of 250 to 300 mg q.d. Khella works synergistically with hawthorn.


    Contents

    Early symptoms of hepatovirus A infection can be mistaken for influenza, but some sufferers, especially children, exhibit no symptoms at all. Symptoms typically appear 2-6 weeks (the incubation period) after the initial infection. [11] About 90% of children do not have symptoms. The time between infection and symptoms, in those who develop them, is 2-6 weeks, with an average of 28 days. [2]

    The risk for symptomatic infection is directly related to age, with more than 80% of adults having symptoms compatible with acute viral hepatitis and the majority of children having either asymptomatic or unrecognized infections. [12]

    Symptoms usually last less than 2 months, although some people can be ill for as long as 6 months: [13]

    Extrahepatic manifestations Edit

    Joint pains, red cell aplasia, pancreatitis and generalized lymphadenopathy are the possible extrahepatic manifestations. Kidney failure and pericarditis are very uncommon. [15] If they occur, they show an acute onset and disappear upon resolution of the disease. [ citation needed ]

    • Hepatitis A virus[16]
    • Human hepatitis A virus[17]
    • Simian hepatitis A virus[17]

    Taxonomy Edit

    Hepatovirus A is a species of virus in the order Picornavirales, family Picornaviridae, genus Hepatovirus. Humans and other vertebrates serve as natural hosts. [18] [19]

    Nine members of Hepatovirus are recognized. [20] These species infect bats, rodents, hedgehogs, and shrews. Phylogenetic analysis suggests a rodent origin for Hepatitis A.

    A member virus of hepatovirus B (Phopivirus) has been isolated from a seal. [21] [22] This virus shared a common ancestor with Hepatovirus A about 1800 years ago. [ citation needed ]

    Another hepatovirus - Marmota himalayana hepatovirus - has been isolated from the woodchuck Marmota himalayana. [23] This virus appears to have had a common ancestor with the primate-infecting species around 1000 years ago. [ citation needed ]

    Genotypes Edit

    One serotype and seven different genetic groups (four human and three simian) have been described. [24] The human genotypes are numbered I–III. Six subtypes have been described (IA, IB, IIA, IIB, IIIA, IIIB). The simian genotypes have been numbered IV–VI. A single isolate of genotype VII isolated from a human has also been described. [25] Genotype III has been isolated from both humans and owl monkeys. Most human isolates are of genotype I. [26] Of the type I isolates subtype IA accounts for the majority.

    The mutation rate in the genome has been estimated to be 1.73–9.76 × 10 −4 nucleotide substitutions per site per year. [27] [28] The human strains appear to have diverged from the simian about 3600 years ago. [28] The mean age of genotypes III and IIIA strains has been estimated to be 592 and 202 years, respectively. [28]

    Structure Edit

    Hepatovirus A is a picornavirus it is not enveloped and contains a positive-sense, single-strand of RNA packaged in a protein shell. [24] Only one serotype of the virus has been found, but multiple genotypes exist. [29] Codon use within the genome is biased and unusually distinct from its host. It also has a poor internal ribosome entry site. [30] In the region that codes for the HAV capsid, highly conserved clusters of rare codons restrict antigenic variability. [18] [31]

    Genus Structure Symmetry Capsid Genomic arrangement Genomic segmentation
    Hepatovirus Icosahedral Pseudo T=3 Nonenveloped Linear Monopartite

    Replication cycle Edit

    Vertebrates such as humans serve as the natural hosts. Transmission routes are fecal-oral and blood. [18]

    Following ingestion, HAV enters the bloodstream through the epithelium of the oropharynx or intestine. [32] The blood carries the virus to its target, the liver, where it multiplies within hepatocytes and Kupffer cells (liver macrophages). Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment of the virus to host receptors, which mediates endocytosis. Replication follows the positive-stranded RNA virus replication model. Translation takes place by viral initiation. The virus exits the host cell by lysis and viroporins. Virions are secreted into the bile and released in stool. HAV is excreted in large numbers about 11 days prior to the appearance of symptoms or anti-HAV IgM antibodies in the blood. The incubation period is 15–50 days and risk of death in those infected is less than 0.5%. [ citation needed ]

    Within the liver hepatocytes, the RNA genome is released from the protein coat and is translated by the cell's own ribosomes. Unlike other picornaviruses, this virus requires an intact eukaryotic initiation factor 4G (eIF4G) for the initiation of translation. [33] The requirement for this factor results in an inability to shut down host protein synthesis, unlike other picornaviruses. The virus must then inefficiently compete for the cellular translational machinery, which may explain its poor growth in cell culture. Presumably for this reason, the virus has strategically adopted a naturally highly deoptimized codon usage with respect to that of its cellular host. Precisely how this strategy works is not quite clear yet. [ citation needed ]

    No apparent virus-mediated cytotoxicity occurs, presumably because of the virus' own requirement for an intact eIF4G, and liver pathology is likely immune-mediated.

    Genus Host details Tissue tropism Entry details Release details Replication site Assembly site Transmission
    Hepatovirus Humans vertebrates Liver Cell receptor endocytosis Lysis Cytoplasm Cytoplasm Oral-fecal blood

    Transmission Edit

    The virus spreads by the fecal–oral route, and infections often occur in conditions of poor sanitation and overcrowding. Hepatitis A can be transmitted by the parenteral route, but very rarely by blood and blood products. Food-borne outbreaks are common, [34] and ingestion of shellfish cultivated in polluted water is associated with a high risk of infection. [35] About 40% of all acute viral hepatitis is caused by HAV. [32] Infected individuals are infectious prior to onset of symptoms, roughly 10 days following infection. The virus is resistant to detergent, acid (pH 1), solvents (e.g., ether, chloroform), drying, and temperatures up to 60 °C. It can survive for months in fresh and salt water. Common-source (e.g., water, restaurant) outbreaks are typical. Infection is common in children in developing countries, reaching 100% incidence, but following infection, lifelong immunity results. HAV can be inactivated by chlorine treatment (drinking water), formalin (0.35%, 37 °C, 72 hours), peracetic acid (2%, 4 hours), beta-propiolactone (0.25%, 1 hour), and UV radiation (2 μW/cm 2 /min). HAV can also be spread sexual contact specifically oroanal sexual acts. [ citation needed ]

    In developing countries, and in regions with poor hygiene standards, the rates of infection with this virus are high [36] and the illness is usually contracted in early childhood. As incomes rise and access to clean water increases, the incidence of HAV decreases. [37] In developed countries, though, the infection is contracted primarily by susceptible young adults, most of whom are infected with the virus during trips to countries with a high incidence of the disease [2] or through contact with infectious persons.

    Humans are the only natural reservoir of the virus. No known insect or other animal vectors can transmit the virus. A chronic HAV state has not been reported. [38]

    Although HAV is excreted in the feces towards the end of the incubation period, specific diagnosis is made by the detection of HAV-specific IgM antibodies in the blood. [39] IgM antibody is only present in the blood following an acute hepatitis A infection. It is detectable from 1–2 weeks after the initial infection and persists for up to 14 weeks. The presence of IgG antibodies in the blood means the acute stage of the illness has passed and the person is immune to further infection. IgG antibodies to HAV are also found in the blood following vaccination, and tests for immunity to the virus are based on the detection of these antibodies. [39]

    During the acute stage of the infection, the liver enzyme alanine transferase (ALT) is present in the blood at levels much higher than is normal. The enzyme comes from the liver cells damaged by the virus. [40]

    Hepatovirus A is present in the blood (viremia) and feces of infected people up to 2 weeks before clinical illness develops. [40]

    Hepatitis A can be prevented by vaccination, good hygiene, and sanitation. [6] [41]

    Vaccination Edit

    The two types of vaccines contain either inactivated Hepatovirus A or a live but attenuated virus. [3] Both provide active immunity against a future infection. The vaccine protects against HAV in more than 95% of cases for longer than 25 years. [42] In the United States, the vaccine developed by Maurice Hilleman and his team was licensed in 1995, [43] [44] and the vaccine was first used in 1996 for children in high-risk areas, and in 1999 it was spread to areas with elevating levels of infection. [45]

    The vaccine is given by injection. An initial dose provides protection lasting one year starting 2–4 weeks after vaccination the second booster dose, given six to 12 months later, provides protection for over 20 years. [45]

    The vaccine was introduced in 1992 and was initially recommended for persons at high risk. Since then, Bahrain and Israel have embarked on elimination programmes. [46] Australia, China, Belarus, Italy, Spain, and the United States have started similar programmes. The incidence of hepatitis A where widespread vaccination has been practised has decreased dramatically. In China and the United States, the incidence of hepatitis A has decreased by 90% since 1990. [47] [48]

    In the United States, vaccination of children is recommended at 1 and 2 years of age [1] hepatitis A vaccination is not recommended in those younger than 12 months of age. [49] It is also recommended in those who have not been previously immunized and who have been exposed or are likely to be exposed due to travel. [1] The CDC recommends vaccination against infection for men who have sex with men. [50]

    No specific treatment for hepatitis A is known. Recovery from symptoms following infection may take several weeks or months. Therapy is aimed at maintaining comfort and adequate nutritional balance, including replacement of fluids lost from vomiting and diarrhea. [14]

    In the United States in 1991, the mortality rate for hepatitis A was estimated to be 0.015% for the general population, but ranged up to 1.8 -2.1% for those aged 50 and over who were hospitalized with icteric hepatitis. [51] The risk of death from acute liver failure following HAV infection increases with age and when the person has underlying chronic liver disease. [ citation needed ]

    Young children who are infected with hepatitis A typically have a milder form of the disease, usually lasting 1–3 weeks, whereas adults tend to experience a much more severe form of the disease. [34]


    Contents

    This degree of diversity makes defining synapomorphy (derived common characteristics) for the group extremely difficult, the order being defined on the basis of molecular affinity rather than morphology. However, some characteristics that are prevalent (common traits) represent potential or putative synapomorphies based on ancestral states. These include flowers that are usually radially symmetric and petals that are free. The gynoecium (female reproductive part) generally consists of two carpels (ovary, style and stigma) that are free, at least toward the apex (partially fused bicarpellate gynoecium) and possess a hypanthium (cup shaped basal floral tube). In the androecium (male reproductive part), the stamen anthers are generally basifixed (attached at its base to the filament), sometimes dorsifixed (attached at centre) (see Carlsward et al (2011) Figure 2). Other commonly occurring features are fruit that is generally follicular (formed from a single carpel), seeds with abundant endosperm surrounding the embryo and leaves with glandular teeth at their margins (glandular dentate, see image). Within the Saxifragales, while the families of the woody clade are primarily woody, the primarily herbaceous families of Crassulaceae and Saxifragaceae exhibit woody features as a secondary transition. [5] [6] [7]

    With 15 families, about 100 genera and about 2,470 species, Saxifragales is a relatively small angiosperm order. [3]

    History Edit

    Saxifragales was first described in 1820 by Berchtold and Presl in 1820 as a group of plants, Saxifrageae, with five genera, including Saxifraga, and therefore bear their names as the botanical authority (Bercht. & J.Presl). [8] At times, that authority has also been given to Dumortier, due to a later publication (1829). Dumortier first used the word Saxifragaceae. [9] By the time of John Lindley's The Vegetable Kingdom (1853), the term Saxifragales was in use, which Lindley called an Alliance, containing five families. [10] Later, the Saxifragales were placed in the angiosperm class Dicotyledons, also called Magnoliopsida. [11]

    Phylogeny Edit

    The order Saxifragales has undergone considerable revision in both placement and composition, since the use of molecular phylogenetics, and the use of the modern Angiosperm Phylogeny Group (APG) classification. [1] [12] They are identified as a strongly monophyletic group. [13]

    In the initial APG publication (1998), the Saxifragales were identified within the core eudicots clade but its relationship to other clades was uncertain. The core eudicots consist of the order Gunnerales and a large clade of Pentapetalae (so named for having a synapomorphy of pentamerous (5 part) perianths), the latter representing about 70% of all angiosperms, with eight major lineages. [14] [15] Later (2003), the order was described as "one of the major surprises of molecular phylogenetic analyses of the angiosperms", having elements previously placed in three or four separate subclasses based on morphology. [16] [3] This was eventually resolved in the third APG system (2009) placing Saxifragales as a sister group to the rosids (Rosidae), within the Pentapetalae clade. [17] [18] [19] This large combination has subsequently been given the name superrosids (Superrosidae), representing part of an early diversification of the angiosperms. [3] [1] [20] Among the rosids, they share a number of similarities with the Rosales, particularly Rosaceae, including a hypanthium, five part flowers and free floral parts. [21] As circumscribed, Saxifragales account for 1.3% of eudicot diversity. [22]

    Biogeography and evolution Edit

    Diversification among Saxifragales was rapid, with the extensive fossil record [24] [25] [26] [27] [28] [29] indicating that the order was more diverse and more widespread than an examination of the extant members suggests, with considerable phenotypic diversity occurring early. [2] The earliest fossil evidence is found in the Turonian-Campanian (late Cretaceous), suggesting a minimum age of 89.5 Myr. However, molecular divergence time estimation suggest an earlier time of 102–108 Myr, into the early Cretaceous, for the crown and stem groups respectively. Within the order Saxifragales, the molecular data imply a very rapid initial diversification time of about 6–8 Myr, between 112–120 Myr, with major lineages appearing within 3–6 Myr. [30] [3] [31]

    The ancestral state appears to be woody, as in Peridiscaceae and the woody clade, but is also ancestral to Grossulariaceae. A number of independent transitions to a herbaceous habit occurred in the ancestors of Crassulaceae, Saxifragaceae and the base of the Haloragaceae-Penthoraceae clade (the other two families in Haloragaceae s.l. remaining woody), while other taxa reverted to a woody habit, especially Crassulaceae. Most of Saxifragales have a superior ovary, but some families show frequent transition with inferior or subinferior position, particularly Saxifragaceae and to a lesser extent Hamamelidaceae. Almost all Grossulariaceae have an inferior ovary. The ancestral carpel number is two, with transition to higher numbers, such as four in Haloragaceae s.l. and Peridiscaceae with five in Penthoraceae. The ancestral carpel number for Crassulaceae is five, decreasing to four in Kalanchoe, where it is synapomorphic for the genus, though the most frequent transition in this family is 6–10, but only where stamen number is increased above five. Some Macaronesian taxa (Aeonieae) have 8–12, with up to 32 carpels for Aeonium. [3]

    The ancestral petal number is five, with three major transitions 5 to 0, 5 to 4, 5 to 6–10. Increased petal number is seen in Paeoniaceae and Crassulaceae, particularly where stamen number is also increased. Cercidiphyllum + Daphniphyllum, Chrysosplenium and Altingia are examples of the complete loss of petals. The ancestral stamen:petal ratio is 1, with transitions characterising several clades, e.g. Paeonicaceae+woody clade >2, Crassulaceae 2 (but Crassula 1). Overall there has been a decrease over evolution, but independent of a decrease in petal number, so that it is the stamen number that has decreased. [3] The ancestral habitat appears to be forests, followed by early diversification into desert and aquatic habitats, with shrubland the most recent colonization. [2]

    Species diversification was rapid following a transition from a warmer, wetter Earth in the Eocene (56–40 Myr) to early Miocene (23–16 Myr), to the cooler drier conditions of the mid-Miocene (16–12 Myr). However, this appears to not have coincided with ecological and phenotypic evolution, which are themselves correlated. There is a clear lag, whereby increase in species diversification was followed later by increases in niche and phenotypic lability. [32]

    Subdivision Edit

    The first APG classification (1998) placed 13 families with the order Saxifragales: [33]

    This was subsequently revised to 15, in the fourth version (2016). [1] The Saxifragales families have been grouped into a number of informally named suprafamilial subclades, with the exception of the basal split of Peridiscaceae, which thus forms a sister group with the rest of Saxifragales. The two major ones are (Paeoniaceae + the woody clade of primarily woody families) and the "core" Saxifragales (i.e. the primarily herbaceous families), with the latter subdivided into two further subclades, (Haloragaceae sensu lato + Crassulaceae) and the Saxifragaceae alliance. [3]

    In the clade Haloragaceae sensu lato (s.l.) + Crassulaceae the genera constituting Haloragaceae s.l. are all small, and APG II (2003) proposed merging them into a single larger Haloragaceae s.l., but transferred Aphanopetalum from Cunoniaceae to this group. [16] The Saxifragaceae alliance represents Saxifragaceae together with a number of woody members of the traditional Saxifragaceae sensu Engler (1930). [34] Within this, APG II (2003) proposed placing the two species of Pterostemon that constitute Pterostemonaceae within Iteaceae, and all subsequent versions have maintained this practice. [16] Thus Saxifragales sensu APG II consisted of only 10 families. The third version (2009) added Peridiscaceae (from Malpighiales), as sister to all other families, but re-expanded Haloragaceae to provide for a narrower circumscription, Haloragaceae sensu stricto (s.s.), to give a total of 14 families. APG IV (2016) added the parasitic family Cynomoriaceae to provide a total of 15 families, although its placement within the order remained unclear. [35] [1]

    Of the 15 families included in APG IV, the basal divergence Peridiscaceae underwent radical shifting and recircumscription from 2003 to 2009. Originally, it consisted of two closely related genera, Peridiscus and Whittonia. The APG II system placed the family in Malpighiales, based on a DNA sequence for the rbcL gene from Whittonia. This sequence turned out to be not from Whittonia, but from other plants whose DNA had contaminated the sample. [36] After placement in Saxifragales, it was expanded to include Soyauxia in 2007, [37] and Medusandra in 2009. [38]

    In the first of the subclades of the remaining Saxifragales, Paeoniaceae possesses many unique features and its taxonomic position was controversial for a long time, [39] and Paeonia was placed in Ranunculales, close to Glaucidium, [40] [41] prior to transfer to Saxifragales as sister to the woody clade. [30] [42]

    In the woody clade, the genus Liquidamber was included in Hamamelidaceae until molecular phylogenetic studies showed that its inclusion might make Hamamelidaceae paraphyletic, and was segregated as a separate monotypic family, Altingiaceae in 2008. [30] Cercidiphyllaceae was for a long time associated with Hamamelidaceae and Trochodendraceae and was often thought to be closer to the latter, [43] which is now in the basal eudicot order Trochodendrales. [44] Daphniphyllum was always thought to have an anomalous combination of characters [45] [45] and was placed in several different orders before molecular phylogenetic analysis showed it to belong to Saxifragales. [46]

    In the core Saxifragales, Crassulaceae [47] and Tetracarpaeaceae [48] have been associated with Saxifragaceae, while Penthorum has been associated both with Crassulaceae and Saxifragaceae, [49] before being placed here. Aphanopetalum was often placed in Cunoniaceae, a family in Oxalidales, even though there were good reasons to put it in Saxifragales, [50] and it was subsequently transferred. [51] Haloragaceae was included in Myrtales, [52] before being placed in Saxifragales. [53]

    The other "core" group, the Saxifragaceae alliance comprises four families: Pterostemonaceae, Iteaceae, Grossulariaceae, and Saxifragaceae, [30] which have long been known to be related to each other, but the circumscription of Saxifragaceae has been much reduced and Pterostemonaceae submerged as Pterostemon in Iteaceae. [54]

    Most of the families are monogeneric. Choristylis is now considered a synonym of Itea, but the addition of Pterostemon, gives Iteaceae two genera. [55] Liquidambar and Semiliquidambar are also submerged into Altingia, making Altingiaceae monogeneric. [56] [57] About 95% of the species are in five families: Crassulaceae (1400), Saxifragaceae (500), Grossulariaceae (150–200), Haloragaceae (150), and Hamamelidaceae (100). [22] [30] [58]