There are several ways to manage turf melting out. They include both cultural and chemical.

Turf melting out is caused by the fungal pathogen "Dreschlera poae", in the family Dematiaceae. It is a common problem on turfgrass and affects many different species. The disease infects all parts of the plant most commonly on golf course roughs, sports fields, and home lawns. There are two stages of the disease: the leaf blade infection and the crown and root infection Melting out occurs during the cool weather of April and May and is encouraged by high nitrogen fertility. The disease is spread by wind-blown or water splashed spores and survive in thatch.

Red thread disease is a fungal infection found on lawns and other turfed areas. It is caused by the corticioid fungus "Laetisaria fuciformis" and has two separate stages. The stage that gives the infection its name is characterised by very thin, red, needle-like strands extending from the grass blade. These are stromata, which can remain viable in soil for two years. After germinating, the stromata infect grass leaf blades through their stomata. The other stage is visible as small, pink, cotton wool-like mycelium, found where the blades meet. It is common when both warmth and humidity are high.

Environment

"Laetisaria fuciformis", the fungus that causes red thread disease develops more often in cool (59-77°F) and wet conditions. These conditions are more present in the spring and fall when rainfall is higher and temperatures are slightly lower. Turf grass that is poor in nutrition and are slow growing are areas that are more susceptible to red thread disease. The fungus grows from the thread like red webbing structures called sclerotia. The sclerotia can survive in leaf blades, thatch, and soil for months to years. These areas that have been infected spread the disease by water, wind, and contaminated equipment. Since this fungus can survive for long periods of time it is essential to cure the infected area so further spreading of the disease does not occur.

Management

Managing red thread disease first starts by providing conditions that are not favorable for the fungal disease to develop. Having a balanced and adequate nitrogen fertilization program helps suppress the disease. This includes applying mild to substantial amounts of phosphorus and potassium to the turf. Other than properly fertilizing the turf, it is very important to maintain a soil pH between 6.5 and 7. Having a more basic pH creates less favorable conditions for a fungus to form. Reducing shade on turf areas also reduces chances of the fungal disease to form because shaded areas create a higher humidity near the turfs surface. Another technique to suppressing red thread disease is top dressing with compost. Suppression of the disease increases with the increase of compost used on the turf. Fungicides are not recommended to control red thread because the cost of chemical control is expensive and turf grasses usually recover from the disease quickly. If the use of fungicides is necessary, products containing strobilurins can be applied and can be very effective if applied before symptoms occur.

Hosts and symptoms

The hosts of the red thread disease only include turf grass. Turf grass is primarily present on home lawns and athletic fields. Some of these turf grass species include annual bluegrass, creeping bentgrass, Kentucky bluegrass, pereninial ryegrass, fine fescue, and bermudagrass. These species of grass are not the only types of turf that can be diagnosed with red thread disease but are the most common hosts. Noticeable symptoms of red thread disease are irregular yellow patches on the turf that are 2 to 24 inches in diameter. Affected areas are diagnosed with faintly pinkish web like sclerotia on the leaf blades. This sclerotia is the fungus growing on the leaf blades. This sclerotia has a reddish to pink spider web look to it.

Necrotic ring spot is a common disease of turf caused by soil borne fungi (Ophiosphaerella korrae) that mainly infects roots (4). It is an important disease as it destroys the appearance of turfgrasses on park, playing fields and golf courses. Necrotic Ring Spot is caused by a fungal pathogen that is an ascomycete that produces ascospores in an ascocarp (6). They survive over winter, or any unfavorable condition as sclerotia. Most infection occurs in spring and fall when the temperature is about 13 to 28°C (5). The primary hosts of this disease are cool-season grasses such as Kentucky bluegrass and annual bluegrass (6). Once turf is infected with "O. korrae", it kills turf roots and crowns. Symptoms of the disease are quite noticeable since they appear as large yellow ring-shaped patches of dead turf. Management of the disease is often uneasy and requires application of multiple controls. The disease can be controlled by many different kind of controls including chemicals and cultural.

Bacterial wilt of turfgrass is the only known bacterial disease of turf. The causal agent is the Gram negative bacterium Xanthomonas campestris pv. graminis. The first case of bacterial wilt of turf was reported in a cultivar of creeping bentgrass known as Toronto or C-15, which is found throughout the midwestern United States. Until the causal agent was identified in 1984, the disease was referred to simply as C-15 decline. This disease is almost exclusively found on putting greens at golf courses where extensive mowing creates wounds in the grass which the pathogen uses in order to enter the host and cause disease.

Creeping bentgrass ("Agrostis stolonifera") and annual bluegrasses ("Poa annua") are the makeup of most putting greens, as well as the preferred hosts of this pathogen. Specifically, Toronto (C-15), Seaside, and Nemisilla are the cultivars of creeping bentgrass most commonly affected. The bacteria enter the plant host and interfere with water and nutrient flow, causing the plant to look drought stressed and to take on a blueish-purple color. Additionally, symptoms of bacterial wilt of turf grass include yellow leaf spots, tan or brown spots, water soaked lesions, elongated yellow leaves and shriveling of aforementioned blue or dark green leaves.Since putting greens are not a pure stand of turf, some grass blades may be resistant to the bacterium and thus remain unharmed while the surrounding turf dies, rendering the putting surface inconsistent and unsightly, especially at high-end golf courses.

Snow mold is a type of fungus and a turf disease that damages or kills grass after snow melts, typically in late winter. Its damage is usually concentrated in circles three to twelve inches in diameter, although yards may have many of these circles, sometimes to the point at which it becomes hard to differentiate between different circles. Snow mold comes in two varieties: pink or gray. While it can affect all types of grasses, Kentucky bluegrass and fescue lawns are least affected by snow mold.

Necrotic ring spot can be managed through chemical and cultural controls. Cultural control includes the use of ammonium sulfate or other acidifying fertilizers to suppress the pathogen by lowering the pH of the soil to between 6.0 and 6.2. The more acidic soil discourages the activity of "O. korrae" (9) When reducing pH to these levels, additional manganese applications should be undertaken to compensate for lower pH. As of now, there are only two resistant cultivars of bluegrass, which are ‘Riviera’, and ‘Patriot’ (9). One component of their resistance could be that they are tolerant to low temperature, because the grass is more susceptible to the pathogen under colder temperatures(8). In addition, reducing watering inputs and growing turf on well drained soils can lessen disease symptoms.

Many different fungicides are used to control the pathogen, Fenarimol, Propiconazole, Myclobutanil, and Azoxystrobin (8). Historically, Fenarimol and Myclobutanil were predominantly used (14). In a study where diluted pesticides were sprayed throughout infested test plots, Fenarimol was found to be the most effective with a 94.6% reduction of the disease. Myclobutanil also decreased the amount of disease, but only by 37.7% (8). Myclobutanil is generally recognized as a very weakly acting demethylation inhibitor (DMI) fungicide and fenarimol is no longer registered for turf so a number of other DMI fungicides have been employed successfully, including Propiconazole, Tebuconazole, Metconazole and others. Pyraclostrobin and Fluoxastrobin have also been used to control the pathogen.

http://www.lawnandmower.com/red-thread-disease.aspx

http://www.grassclippings.co.uk/RedThread.pdf

As snow mold remains dormant during summer months when other forms of disease fungi are most active, steps to prevent snow mold infestations must be taken near the end of the summer months. While active lawn care such as regular mowing and raking of leaves is typically sufficient to prevent an infestation, the use of chemicals may sometimes be required. Fungicides, which should typically be applied immediately prior to the first large snowfall in an area, can be used if typical cultural methods do not work.

Lethal yellowing (LY) is a phytoplasma disease that attacks many species of palms, including some commercially important species such as the coconut and date palm. In the Caribbean it is spread by the planthopper "Haplaxius crudus" (former name "Myndus crudus") which is native to Florida, parts of the Caribbean and Central America. The only effective cure is prevention, i.e. planting resistant varieties of coconut palm and preventing a park or 'golf course like' environments which attracts the planthopper. Some cultivars, such as the Jamaica Tall coconut cultivar, nearly died out by lethal yellowing. Heavy turf grasses and similar green ground cover will attract the planthopper to lay its eggs and the nymphs develop at the roots of these grasses. The planthoppers' eggs and nymphs may pose a great threat to coconut growing countries' economies, into which grass seeds for golf courses and lawns are imported from the Americas.

It is not clearly understood how the disease was spread to East Africa as the planthopper "Haplaxius crudus" is not native in East Africa.

The only explanation is that it was imported with grass seed from Florida that was used to create golf courses and lawns in beach resorts. There is a direct connection between green lawns and the spread of lethal yellowing in Florida. Even so-called 'resistant cultivars' such as the Malayan Dwarf or the Maypan hybrid between that dwarf and the Panama Tall were never claimed to have a 100% immunity. The nymphs of the planthoppers develop on roots of grasses, hence the areas of grass in the vicinity of palm trees is connected with the spread of this phytoplasma disease. The problem arose as a direct result of using coconut and date palms for ornamental and landscaping purposes in lawns, golf courses and gardens together with these grasses. When these two important food palms were grown in traditional ways (without grasses) in plantations and along the shores, the palm groves were not noticeably affected by lethal yellowing. There is no evidence that disease can be spread when instruments used to cut an infected palm are then used to cut or trim a healthy one. Seed transmission has never been demonstrated, although the phytoplasma can be found in coconut seednuts, but phytosanitary quarantine procedures that prevent movement of coconut seed, seedlings and mature palms out of an LY epidemic area should be applied to grasses and other plants that may be carrying infected vectors.

Beside coconut palm ("Cocus nucifera"), more than 30 palm species have also been reported as susceptible to lethal phytoplasmas around the globe.

Dutch elm disease (DED) is caused by a member of the sac fungi (Ascomycota) affecting elm trees, and is spread by elm bark beetles. Although believed to be originally native to Asia, the disease was accidentally introduced into America and Europe, where it has devastated native populations of elms that did not have resistance to the disease. It has also reached New Zealand. The name "Dutch elm disease" refers to its identification in 1921 and later in the Netherlands by Dutch phytopathologists Bea Schwarz and Christine Buisman who both worked with Professor Johanna Westerdijk. The disease affects species in the genera "Ulmus" and "Zelkova", therefore it is not specific to the Dutch elm hybrid.

The causative agents of DED are ascomycete microfungi. Three species are now recognized:

- "Ophiostoma ulmi", which afflicted Europe from 1910, reaching North America on imported timber in 1928.

- "Ophiostoma himal-ulmi", a species endemic to the western Himalaya.

- "Ophiostoma novo-ulmi", an extremely virulent species from Japan which was first described in Europe and North America in the 1940s and has devastated elms in both continents since the late 1960s.

DED is spread in North America by three species of bark beetles (Family: Curculionidae, Subfamily: Scolytinae):

- The native elm bark beetle, "Hylurgopinus rufipes".

- The European elm bark beetle, "Scolytus multistriatus".

- The banded elm bark beetle, "Scolytus schevyrewi".

In Europe, while "S. multistriatus" still acts as a vector for infection, it is much less effective than the large elm bark beetle, "S. scolytus". "H. rufipes" can be a vector for the disease, but is inefficient compared to the other vectors. "S. schevyrewi" was found in 2003 in Colorado and Utah.

Other reported DED vectors include "Scolytus sulcifrons", "S. pygmaeus", "S. laevis", "Pteleobius vittatus" and "Р. kraatzi". Other elm bark beetle species are also likely vectors.

As of November 2013, no identifiable cause for the disease had been found. Pathogenic bacteria did not seem to be present, and though the plague might be caused by a viral or fungal pathogen, no causal agent had been found. Each episode of plague might have a different cause.

Other possible causes of the condition that have been suggested include high sea temperatures, oxygen depletion and low salinity due to freshwater runoff. Research suggests that high water temperatures are indeed linked to the disease, increasing its incidence and virulence. The disease also seems more prevalent in sheltered waters than in open seas with much wave movement. One result of global warming is higher sea temperatures. There is a wave of unusually warm water along the west coast of the United States, which is where all of the sea stars are dying off. These may impact both on starfish and on echinoderm populations in general, and a ciliate protozoan parasite ("Orchitophrya stellarum") of starfish, which eats sperm and effectively emasculates male starfish, thrives at higher temperatures.

Research in 2014 showed that the cause of the disease is transmissible from one starfish to another and that the disease-causing agent is a microorganism in the virus-size range. The most likely candidate causal agent was found to be the sea star-associated densovirus (SSaDV), which was found to be in greater abundance in diseased starfish than in healthy ones.

In 2014, Point Defiance Zoo and Aquarium lost more than half of its 369 sea stars, and by September 2015 they numbered fewer than 100. The aquarium treated its affected sea stars with antibiotics in 2014, which proved effective. Although a mechanism is still unknown, evidence suggests that a single mutation in the elongation factor 1-alpha locus in "Pisaster ochraceus" may be associated with reduced mortality.

Treatment for horses with thrush includes twice-daily picking of the feet, taking special care to clean out the two collateral grooves and the central sulcus. The feet may then be scrubbed clean using a detergent and/or disinfectant and warm water, before the frog is coated with a commercial thrush-treatment product, or with iodine solution, which may be soaked into cotton balls and packed into the clefts. Several home remedies are used, such as a hoof packing of a combination of sugar and betadine, powdered aspirin, borax, or diluted bleach. It is best, however, to speak with the horse's veterinarian, to be sure these home remedies are effective and, more importantly, safe for use on horses.

Horses with thrush, or those at risk for contracting it, are best kept in a dry, clean environment. Daily cleaning of the hooves also contributes to the prevention of thrush. In general, thrush is relatively easy to treat, although it can easily return and it can take up to a year for a fully healthy frog to regrow after a severe infection.

The most obvious sign of thrush is usually the odor that occurs when picking out the feet. Additionally, the infected areas of the hoof will be black in color (even on a dark-horned hoof), and will easily break or crumble when scraped with a hoof pick. When picking the hooves around thrush areas, the differences between healthy and infected areas can be seen when white/gray tissue (healthy frog) is surrounding a dark, smelly (infected) area.

Most horses do not become lame if infected with thrush. However, if left untreated, the bacteria may migrate deeper into the sensitive parts of the hoof, which will result in lameness. Then, the horse may also react when its feet are picked out, and blood may be seen.

Research is looking into connections between hair loss and other health issues. While there has been speculation about a connection between early-onset male pattern hair loss and heart disease, a review of articles from 1954 to 1999 found no conclusive connection between baldness and coronary artery disease. The dermatologists who conducted the review suggested further study was needed.

Environmental factors are under review. A 2007 study indicated that smoking may be a factor associated with age-related hair loss among Asian men. The study controlled for age and family history, and found statistically significant positive associations between moderate or severe male pattern hairloss and smoking status.

Vertex baldness is associated with an increased risk of coronary heart disease (CHD) and the relationship depends upon the severity of baldness, while frontal baldness is not. Thus, vertex baldness might be a marker of CHD and is more closely associated with atherosclerosis than frontal baldness.

Other causes of hair loss include:

- Alopecia mucinosa

- Biotinidase deficiency

- Chronic inflammation

- Diabetes

- Lupus erythematosus

- Pseudopelade of Brocq

- Telogen effluvium

- Tufted folliculitis

The following measures are advisable for keeping the vulva and vagina healthy:

- Avoiding washing with soap, since soap disturbs the natural pH balance of the vagina. Some pH-balanced soaps exist, but their effects remain unclear. Other measures are seldom necessary or advisable. Two notable examples: so-called "feminine hygiene sprays" are unnecessary, may be generally harmful, and have been known to cause severe allergic reactions. Vaginal douching is generally not necessary and has been implicated in helping to cause bacterial vaginosis (BV) and candidiasis ("yeast infections").

- After using the toilet, wipe from the front toward the back to avoid introducing bacteria from the anal area into the vulva. Use non-perfumed, undyed toilet paper.

- Drink plenty of water and urinate frequently and as soon as possible when you feel the need, to help flush bacteria out of the urinary tract and avoid urinary tract infections. For the same reason, try to urinate before and after sex.

- Change out of a wet swimsuit or other wet clothes as soon as possible.

- Avoid fragrances, colours, and "deodorants" in products that contact the vulva/vagina: sanitary napkins, tampons, and toilet paper. Some women who are sensitive to these substances should also avoid bubble baths and some fabric detergents and softeners.

- Use a menstrual cup instead of sanitary pads or tampons. Menstrual cups are a new form of menstrual product that has recently been rapidly gaining in popularity as a greener, more cost-effective and healthier alternative to tampons and sanitary pads.

- Avoid wearing leather trousers, tight jeans, panties made of nylon or other synthetic fabrics, or pantyhose without an all-cotton crotch (not cotton covered by nylon - cut out the nylon panel if necessary).

- Anything which has been in contact with the anal area (see anal sex) should be thoroughly washed with soap and water or a disinfectant before coming in contact with the vulva or vagina.

- Use condoms during heterosexual intercourse, practise safer sex, know your sex partners, ask sex partners to practise basic hygiene of their genitals. Use artificial lubrication during the intercourse if the amount naturally produced is not enough.

- Be careful with objects inserted inside the vagina. Improper insertion of objects into any body opening can cause damage: infection, cutting, piercing, trauma, blood loss, etc.

- Avoid letting any contaminants inside the vagina, including dirt but especially sand.

- See your gynecologist regularly.

- Be careful while removing hair in this area.

Women who are unable to walk are more likely to have infections. The problem can be prevented according to above-mentioned and following measures:

- Wash crotch and rectal areas (with a soap-substitute if desired) and large amount of warm running water, every morning and evening. The disabled person can sit on a shower chair with an open seat or on a toilet. Use a shower head or water container to wash more directly.

- Use towel to dry.

- DO NOT use talcum/body powder, if desired use corn starch powder (corn-flour) on the skin of the genital area to absorb perspiration.

- Avoid sitting on plastic or synthetic materials for extended lengths of time.

- Wear loose underpants and change if soilage or wetness occurs.

Research has shown that there are five million teeth knocked-out each year in the United States.

Up to 25% of school-aged children and military trainees and fighters experience some kind of dental trauma each year. The incidence of dental avulsion in school aged children ranges from 0.5 to 16% of all dental trauma. Many of these teeth are knocked-out during school activities or sporting events such as contact sports, football, basketball, and hockey.It is important for anyone whom is related, working, or witnessing sports that they be educated on this subject matter. Being educated could aid in minimizing injuries that could do further harm to the victim. Being informed and spreading awareness of dental avulsion in the state of knowledge, treatment, and prevention could make an impact.

Vulvovaginal health is the health and sanitation of the human vulva and vagina.

Problems affecting this area include vulva diseases, vaginal diseases and urinary tract infections.

Thallium and its compounds are often highly toxic. Contact with skin is dangerous, and adequate ventilation should be provided when melting this metal. Many thallium(I) compounds are highly soluble in water and are readily absorbed through the skin. Exposure to them should not exceed 0.1 mg per m of skin in an 8-hour time-weighted average (40-hour work week). Thallium is a suspected human carcinogen.

Part of the reason for thallium's high toxicity is that, when present in aqueous solution as the univalent thallium(I) ion (Tl), it exhibits some similarities with essential alkali metal cations, particularly potassium (due to similar ionic radii). It can thus enter the body via potassium uptake pathways. Other aspects of thallium's chemistry differ strongly from that of the alkali metals, such as its high affinity for sulfur ligands. Thus, this substitution disrupts many cellular processes (for instance, thallium may attack sulfur-containing proteins such as cysteine residues and ferredoxins). Thallium's toxicity has led to its use (now discontinued in many countries) as a rat and ant poison.

Among the distinctive effects of thallium poisoning are hair loss (which led to its initial use as a depilatory before its toxicity was properly appreciated) and damage to peripheral nerves (victims may experience a sensation of walking on hot coals), although the loss of hair only generally occurs in low doses; in high doses the thallium kills before this can take effect. Thallium was once an effective murder weapon before its effects became understood and an antidote (Prussian blue) discovered. Indeed, thallium poisoning has been called the "poisoner's poison" since thallium is colorless, odorless and tasteless; its slow-acting, painful and wide-ranging symptoms are often suggestive of a host of other illnesses and conditions.

Copper toxicity, also called copperiedus, refers to the consequences of an excess of copper in the body. Copperiedus can occur from eating acid foods cooked in uncoated copper cookware, or from exposure to excess copper in drinking water, as a side-effect of estrogen birth control pills, or other environmental sources. It can also result from the genetic condition Wilson's disease.

The long-term prognosis of replanted knocked out teeth is very variable. The treatment for knocked-out teeth has progressed from a success rate of 10% to over 90%.

However, this success rate can only be achieved with the institution of optimum care within fifteen minutes to an hour of the accident. In the case of knocked-out teeth, being prepared and knowing what to do can mean the difference between a person retaining or losing replanted knocked-out teeth for life. Teeth that have been knocked out when they are fully matured, that is, when the root has completely formed, have a much better prognosis than those teeth that are immature and not fully formed. This is due to the fragility of the root. When teeth have not fully formed, the walls of the root are thinner and thus more fragile. Another complication for the prognosis is the length of time that the tooth has been out of its socket. Teeth that are replanted within fifteen minutes of the accident have an excellent prognosis. Teeth that have been extra-oral and dry stored for more than one hour have a poor prognosis. Teeth that have been placed in an optimal storage medium within one hour of the accident also have an excellent prognosis. All teeth that have been knocked out should be replanted but watched carefully for the development of root resorption. Teeth that do not have root canal treatment within two weeks of replantation also have a poor prognosis.