Cold Sores in the Nose

If you don’t stop cold sores in the nose before they start, or halt them in there tracks, you are in for a long two weeks.

Cold sores usually appear on the lips and areas around the mouth. But sometimes they can appear on the cheeks, the nose and in your nostrils. This may occur because the virus, which travels through nerve paths, can find its way to other areas of your face; if these areas are near the initial vicinity of infection.

Getting cold sores in the nose can be more painful than the ones that generally appear on the lips and around the mouth.

Cold sores blisters in the nose are similar to those that appear on your lips and mouth. They swell and form blisters which erupt, produce scabbing and finally heal, usually leaving no scars.

This is called “nasal herpes”. Basically, the virus goes through the same stages that oral herpes goes through; that of the ‘prodrome’ stage, the ‘weeping’ stage and the ‘healing’ stage.

· The ‘prodrome’ stage consists of feeling a burning or tingling sensation followed by a formation of small blisters at the site of infection.

· Next is the ‘weeping’ stage wherein the blister starts to ooze and crust over into a scab.

· Finally, in the ‘healing’ stage where new skin replaces the scab.

Cold sores in the nose can be a result of ‘autoinoculation’.

This is when you spread the virus from one area to another such as; by touching your nose after touching a cold sore. Being conscious of what you touch and where your hands have been will help avoid spreading the virus to other parts of your body.

Washing your hands often with soap and water will also help prevent autoinoculation.

Cold sores in the nose, can be painful, particularly if you simultaneously have the flu or a cold. The conditions inside the nose, being moist and warm, cause the virus to multiply, thereby increasing its chances to infect nearby areas.

This moistness also leads to a longer healing time than usual. The cold sores are aggravated every time you blow or wipe your nose.

When the scabbing stage begins, the crust of the scab becomes hard due to the constant flow of air in the nostrils.

This means the scab can easily break and bleed with just a movement of your nose. The skin in the nostrils is fragile and thin which increases the possibility of the scabs breaking and bleeding easily. This may then promote further infection of the virus.

Applying home remedies, like ice, can help relieve the pain of the cold sores or fever blisters and speed up the healing time. Taking L-lysine can also shorten the duration of the episode.

Having cold sores or fever blisters on any part of the face is unpleasant enough. But having cold sores in the nose could possibly be the worst.

The best solution is to stop the cold sore in its tracks or even prevent it from forming at all. That way you don’t have to deal with cold sores in the nose at all. This can be done effectively with vitamins and supplements.

Psoriasis – We Can not Change Our Genetics, But We Can Eliminate Stress

Presently genetic psoriasis theory is one of the most reliable psoriasis theories.

But genetic predisposition alone is not enough for the development of psoriasis. There has to be some kind of a trigger to start the mechanisms of psoriasis.

Let's discuss what stress is, and what stress may cause in the genetically predisposed to psoriasis people.

Stress is usually a strong negative (rarely – positive) mental or physical experience, which causes various negative chemical reactions in our body.

These chemical reactions are capable of deteriorating the internal organs of our body, and causing various physical disorders as well as various disorders of the nervous system. Most of these disorders would never have surfaced, had they not been triggered by stress.

In the same way stress may eventually also trigger the pathological mechanisms of psoriasis disease.

Various studies have shown that stress is one of the most often psoriasis triggers in the genetically predisposed to psoriasis people – about 50% of the cases. Stress is also a major factor for the flare up of psoriasis – about 40% of the cases.

Therefore, it would be a prudent thing to do to try to avoid getting stressed, or to learn to relieve your everyday stress.

Mental stress may be often caused by losing your loved ones, losing your job, getting divorced etc …

Physical stress may be often caused by freezing, getting into a car accident, undergoing a major surgery etc …

Stress may also be caused by a positive experience, such as getting married or giving birth to a child.

In order to try to prevent psoriasis in the predisposed to psoriasis adults and children, or to better manage the existing psoriasis, I would advise you to screen your life or your child's life for any possible causes of stress.

It is easier for an adult to find the possible causes of stress but it may be harder to do that for a child.

Here is the list of things you may want to look for in your child's life:
-Skipping Meals;
-Dressing Improperly;
-Having A conflict at school or in preschool;
-Insufficient Sleep or not enough rest;
-Uncomfortable Clothes or footwear.

By trying to eliminate stress, we may as well succeed in preventing psoriasis or improving the developed psoriasis. It is definitely worth a try.

Here are the most often symptoms of stress, both in the adults and in children:
-Feeling Down;
-Fast Heartbeat;

Thus, if you find anything that may be stressing you (or your child) you should try to eliminate it, especially if this turns out to have been a prolonged stress.

There are various relaxation techniques, which may help you in your stress management.

Chiropractic & Low Back Pain

Low back pain is probably the most common pain to afflict the human race. During the lifetime of anyone of us, this is likely to occur on certainly more than one occasion. The human frame consists of a skeletal framework that we call the spine, In turn the spine is made up of 24 individual bones or vertebrae and between each vertebra is a disc which acts as a shock absorber.

Without these discs the bones would quickly wear out and fracture from everyday forces such as jumping off the back of a truck. Between the discs are the spinal nerve roots which in sprout off from off the spinal cord. The spinal cord is a continuation of the brain and commences at the base of the skull and continues right down to the “tail bone”.

There are seven layers of muscles which support the spine and help keep us upright. Now that we have had this mini-lesson of anatomy, we can get some idea of just how complex the musculoskeletal system is. No wonder that low back pain occurs so frequently when we are so reliant on all of the above systems to keep us straight and active.

The spinal nerve roots are incredibly sensitive to changes of posture and position and register pain if they are in way squeezed or impinged. While we prefer not to actually call it a pinched nerve, the pain that occurs certainly feels as if the nerve is having just that done to it. In addition the vertebrae of the low back, which we call lumbar vertebrae, have small facet joints which also have nerve endings and are sensitive to pain.

When irritation occurs, either directly from spinal nerves being impinged or from facet joints being fixated (subluxated), pain occurs in the low back. The muscles of the spine which were referred to previously, receive their nerve supply from the same nerves that exit from the spinal cord, between the vertebrae.

These muscles contract and go into painful spasm when their nerve supply is compromised. They do this as a reflex action to protect the affected area and the result can be very painful. The sciatic nerve is a large nerve which is made up of five individual spinal nerves of the low back. The sciatic nerve passes through the buttock (gluteal) region and descends down both legs. There is a sciatic nerve on each side of the body.

The term “sciatica” refers to the very painful condition which occurs when one or more of the five nerve roots become impinged. Both pain and numbness or tingling of the nerves can take place from the gluteal region, right down to the legs, feet and toes. In addition, as I have already mentioned, the muscles receive their nerve innervation from those very same nerves

Those muscles can become weak and in some cases, atrophied. This means that a leg muscle will become thinner and weaker on one side when compared to the other leg muscle. Referred pain has now occurred with the initial point of nerve pressure at the lumbar spinal region now having a direct effect on a distant area, such as the toes and feet.

As a chiropractor of some twenty five years experience, I advise my patients who present with this problem to have x rays and possibly an MRI or CT scan. This will then form the basis of my orthopedic and neurological examination after which an accurate diagnosis can be made. If appropriate, chiropractic treatment can then be commenced and the patient started on the road to recovery.

In addition to the chiropractic treatment which might take place twice weekly over some weeks, the patient will be instructed how to perform exercises to strengthen both back muscles and the intrinsic core muscles of the body. This will ensure upright posture and spinal stability. There is absolutely no need for a person to put up with low back pain for the rest of their life when gentle and effective chiropractic care is readily available.

Allergy – Causes and Symptoms

An allergy can be defined as the hyperactive response taking place in the immune system when subjected to a foreign substance. The substance which causes allergies is termed as allergens. There are so many types of allergens such as food, dust, pollen and so on. The allergy treatments are directed at suppressing the functioning of immune system with steroids. Drug and sting of insects can also be considered as one of the allergens for producing the respiratory allergy. In short, we can say that allergies occurs when the immune systems gives a wrong signal.

The allergies may cause so many kinds of side effects, which may worsen the person's health. Allergies are more common during the winter and spring season.

Mostly in children, the consumption of fat forms an important reason for developing the allergic disease. The fatty acids such as margarine are considered to endorse the prostaglandin E2 formation which in turn will affect the immune system thereby enhancing the allergic reactions. Butter is the best example for the margarine fats.

Running nose is one of the mild effects of allergy which turns into asthma in the worst cases. Asthma occurs when the dust or pollen are inhaled into the lungs. Pollen allergies are considered to be seasonal allergens .The harmless reaction occurs mostly in the non-allergic people. The other symptoms of allergies are redness in the eyes, blurred vision and itchy eyes which increases the amount of tears. There are so many researches conducted for finding out the allergy treatments. In most cases, the treatments are given by blocking the response of the immune system.

Drosophila Melanogaster

Physical appearance

Male (left) and female D. melanogaster

Wildtype fruit flies have brick red eyes, are yellow-brown in color, and have transverse black rings across their abdomen. They exhibit sexual dimorphism: females are about 2.5 millimeters (0.1 inches) long; males are slightly smaller and the back of their bodies is darker. Males are easily distinguished from females based on color differences, with a distinct black patch at the abdomen, less noticeable in recently emerged flies (see fig), and the sexcombs (a row of dark bristles on the tarsus of the first leg). Furthermore, males have a cluster of spiky hairs (claspers) surrounding the reproducing parts used to attach to the female during mating. There are extensive images at FlyBase.

Life cycle and reproduction

Egg of D. melanogaster

The D. melanogaster lifespan is about 30 days at 29 C (84 F).

The developmental period for Drosophila melanogaster varies with temperature, as with many ectothermic species. The shortest development time (egg to adult), 7 days, is achieved at 28 C (82 F). Development times increase at higher temperatures (30 C (86 F), 11 days) due to heat stress. Under ideal conditions, the development time at 25 C (77 F) is 8.5 days, at 18 C (64 F) it takes 19 days and at 12 C (54 F) it takes over 50 days. Under crowded conditions, development time increases, while the emerging flies are smaller. Females lay some 400 eggs (embryos), about five at a time, into rotting fruit or other suitable material such as decaying mushrooms and sap fluxes. The eggs, which are about 0.5 millimetres long, hatch after 1215 hours (at 25 C (77 F)). The resulting larvae grow for about 4 days (at 25 C) while molting twice (into 2nd- and 3rd-instar larvae), at about 24 and 48 h after hatching. During this time, they feed on the microorganisms that decompose the fruit, as well as on the sugar of the fruit itself. Then the larvae encapsulate in the puparium and undergo a four-day-long metamorphosis (at 25 C), after which the adults eclose (emerge).

Mating fruit flies. Note sexcombs male insert.

Females become receptive to courting males at about 812 hours after emergence. Males perform a sequence of five behavioral patterns to court females. First, males orient themselves while playing a courtship song by horizontally extending and vibrating their wings. Soon after, the male positions itself at the rear of the female’s abdomen in a low posture to tap and lick the female genitalia. Finally, the male curls its abdomen, and attempts copulation. Females can reject males by moving away and extruding their ovipositor. The average duration of successful copulation is 30 minutes, during which males transfer a few hundred very long (1.76 mm) sperm cells in seminal fluid to the female. Females store the sperm in a tubular receptacle and in two mushroom-shaped spermathecae, sperm from multiple matings compete for fertilization. A last male precedence is believed to exist in which the last male to mate with a female sires approximately 80% of her offspring. This precedence was found to occur through displacement and incapacitation.. The displacement is attributed to sperm handling by the female fly as multiple matings are conducted and is most significant during the first 12 days after copulation. Displacement from the seminal receptacle is more significant than displacement from the spermathecae. Incapacitation of first male sperm by second male sperm becomes significant 27 days after copulation. The seminal fluid of the second male is believed to be responsible for this incapacitation mechanism (without removal of first male sperm) which takes effect before fertilization occurs. The delay in effectiveness of the incapacitation mechanism is believed to be a protective mechanism that prevents a male fly from incapacitating its own sperm should it mate with the same female fly repetitively.

History of use in genetic analysis

Drosophila melanogaster was among the first organisms used for genetic analysis, and today it is one of the most widely-used and genetically best-known of all eukaryotic organisms. All organisms use common genetic systems; therefore, comprehending processes such as transcription and replication in fruit flies helps in understanding these processes in other eukaryotes, including humans.

Charles W. Woodworth is credited with being the first to breed Drosophila in quantity and for suggesting to W. E. Castle that they might be used for genetic research during his time at Harvard University. But it was not until 1910 that Thomas Hunt Morgan began using fruit flies in experimental studies of heredity at Columbia University.

Morgan’s laboratory was located on the top floor of Schermerhorn Hall, which became known as the Fly Room. The Fly Room was cramped with eight desks, each occupied by students and their experiments. They started off experiments using milk bottles to rear the fruit flies and handheld lenses for observing their traits. The lenses were later replaced by microscopes which enhanced their observations. The Fly Room was the source of some of the most important research in the history of biology. Morgan and his students eventually elucidated many basic principles of heredity, including sex-linked inheritance, epistasis, multiple alleles, and gene mapping.

“Thomas Hunt Morgan and colleagues extended Mendel’s work by describing X-linked inheritance and by showing that genes located on the same chromosome do not show independent assortment. Studies of X-linked traits helped confirm that genes are found on chromosomes, while studies of linked traits led to the first maps showing the locations of genetic loci on chromosomes” (Freman 214). The first maps of Drosophila chromosomes were completed by Alfred Sturtevant.

Model organism in genetics

D. melanogaster types (clockwise): brown eyes with black body, cinnabar eyes, sepia eyes with ebony body, vermilion eyes, white eyes, and wild-type eyes with yellow body

Drosophila melanogaster is one of the most studied organisms in biological research, particularly in genetics and developmental biology. There are several reasons:

The care and culture requires little equipment and use little space even when using large cultures, and the overall cost is low.

It is small and easy to grow in the laboratory and their morphology is easy to identify once they are anesthetized (usually with ether, carbon dioxide gas, by cooling them, or with products like FlyNap)

It has a short generation time (about 10 days at room temperature) so several generations can be studied within a few weeks.

It has a high fecundity (females lay up to 100 eggs per day, and perhaps 2000 in a lifetime).

Males and females are readily distinguished and virgin females are easily isolated, facilitating genetic crossing.

The mature larvae show giant chromosomes in the salivary glands called polytene chromosomes”puffs” indicate regions of transcription and hence gene activity.

It has only four pairs of chromosomes: three autosomes, and one sex chromosome.

Males do not show meiotic recombination, facilitating genetic studies.

Recessive lethal “balancer chromosomes” carrying visible genetic markers can be used to keep stocks of lethal alleles in a heterozygous state without recombination due to multiple inversions in the balancer.

Genetic transformation techniques have been available since 1987.

Its complete genome was sequenced and first published in 2000.

Genetic markers

Genetic markers are commonly used in Drosophila research, for example within balancer chromosomes or P-element inserts, and most phenotypes are easily identifiable either with the naked eye or under a microscope. In the list of example common markers below, the allele symbol is followed by the name of the gene affected and a description of its phenotype. (Note: Recessive alleles are in lower case, while dominant alleles are capitalised.)

Cy1: curly; The wings curve away from the body, flight may be somewhat impaired.

e1: ebony; Black body and wings (heterozygotes are also visibly darker than wild type).

Sb1: stubble; Hairs are shorter and thicker than wild type.

w1: white; Eyes lack pigmentation and appear white, vision may be somewhat impaired.

y1: yellow; Body pigmentation and wings appear yellow.

Drosophila genes are traditionally named after the phenotype they cause when mutated. For example, the absence of a particular gene in Drosophila will result in a mutant embryo that does not develop a heart. Scientists have thus called this gene tinman, named after the Oz character of the same name. This system of nomenclature results in a wider range of gene names than in other organisms.


D. melanogaster chromosomes to scale with megabase-pair references oriented as in the National Center for Biotechnology Information database. Centimorgan distances are approximate and estimated from the locations of selected mapped loci.

The genome of D. melanogaster (sequenced in 2000, and curated at the FlyBase database) contains four pairs of chromosomes: an X/Y pair, and three autosomes labeled 2, 3, and 4. The fourth chromosome is so tiny that it is often ignored, aside from its important eyeless gene. The D. melanogaster sequenced genome of 165 million base pairs has been annotated and contains approximately 13,767 protein-coding genes which comprise ~20% of the genome out of a total of an estimated 14,000 genes. More than 60% of the genome appears to be functional non-protein-coding DNA involved in gene expression control. Determination of sex in Drosophila occurs by the ratio of X chromosomes to autosomes, not because of the presence of a Y chromosome as in human sex determination. Although the Y chromosome is entirely heterochromatic, it contains at least 16 genes, many of which are thought to have male-related functions.

Similarity to humans

About 75% of known human disease genes have a recognizable match in the genetic code of fruit flies, and 50% of fly protein sequences have mammalian analogues. An online database called Homophila is available to search for human disease gene homologues in flies and vice versa. Drosophila is being used as a genetic model for several human diseases including the neurodegenerative disorders Parkinson’s, Huntington’s, spinocerebellar ataxia and Alzheimer’s disease. The fly is also being used to study mechanisms underlying aging and oxidative stress, immunity, diabetes, and cancer, as well as drug abuse.


Main article: Drosophila embryogenesis

Embryogenesis in Drosophila has been extensively studied, as its small size, short generation time, and large brood size makes it ideal for genetic studies. It is also unique among model organisms in that cleavage occurs in a syncytium.

Drosophila melanogaster oogenesis

During oogenesis, cytoplasmic bridges called “ring canals” connect the forming oocyte to nurse cells. Nutrients and developmental control molecules move from the nurse cells into the oocyte. In the figure to the left, the forming oocyte can be seen to be covered by follicular support cells.

After fertilization of the oocyte the early embryo (or syncytial embryo) undergoes rapid DNA replication and 13 nuclear divisions until approximately 5000 to 6000 nuclei accumulate in the unseparated cytoplasm of the embryo. By the end of the 8th division most nuclei have migrated to the surface, surrounding the yolk sac (leaving behind only a few nuclei, which will become the yolk nuclei). After the 10th division the pole cells form at the posterior end of the embryo, segregating the germ line from the syncytium. Finally, after the 13th division cell membranes slowly invaginate, dividing the syncytium into individual somatic cells. Once this process is completed gastrulation starts.

Nuclear division in the early Drosophila embryo happens so quickly there are no proper checkpoints so mistakes may be made in division of the DNA. To get around this problem the nuclei which have made a mistake detach from their centrosomes and fall into the centre of the embryo (yolk sac) which will not form part of the fly.

The gene network (transcriptional and protein interactions) governing the early development of the fruit fly embryo is one of the best understood gene networks to date, especially the patterning along the antero-posterior (AP) and dorso-ventral (DV) axes (See under morphogenesis).

The embryo undergoes well-characterized morphogenetic movements during gastrulation and early development, including germ-band extension, formation of several furrows, ventral invagination of the mesoderm, posterior and anterior invagination of endoderm (gut), as well as extensive body segmentation until finally hatching from the surrounding cuticle into a 1st-instar larva.

During larval development, tissues known as imaginal discs grow inside the larva. Imaginal discs develop to form most structures of the adult body, such as the head, legs, wings, thorax and genitalia. Cells of the imaginal disks are set aside during embryogenesis and continue to grow and divide during the larval stages – unlike most other cells of the larva which have differentiated to perform specialized functions and grow without further cell division. At metamorphosis, the larva forms a pupa, inside which the larval tissues are reabsorbed and the imaginal tissues undergo extensive morphogenetic movements to form adult structures.

Behavioral genetics and neuroscience

In 1971, Ron Konopka and Seymour Benzer published “Clock mutants of Drosophila melanogaster”, a paper describing the first mutations that affected an animal’s behavior. Wild-type flies show an activity rhythm with a frequency of about a day (24 hours). They found mutants with faster and slower rhythms as well as broken rhythms – flies that move and rest in random spurts. Work over the following 30 years has shown that these mutations (and others like them) affect a group of genes and their products that comprise a biochemical or biological clock. This clock is found in a wide range of fly cells, but the clock-bearing cells that control activity are several dozen neurons in the fly’s central brain.

Since then, Benzer and others have used behavioral screens to isolate genes involved in vision, olfaction, audition, learning/memory, courtship, pain and other processes, such as longevity.

The first learning and memory mutants (dunce, rutabaga etc) were isolated by William “Chip” Quinn while in Benzer’s lab, and were eventually shown to encode components of an intracellular signaling pathway involving cyclic AMP, protein kinase A and a transcription factor known as CREB. These molecules were shown to be also involved in synaptic plasticity in Aplysia and mammals.

Male flies sing to the females during courtship using their wing to generate sound, and some of the genetics of sexual behavior have been characterized. In particular, the fruitless gene has several different splice forms, and male flies expressing female splice forms have female-like behavior and vice-versa.

Furthermore, Drosophila has been used in neuropharmacological research, including studies of cocaine and alcohol consumption.


Stereo images of the fly eye

The compound eye of the fruit fly contains 760 unit eyes or ommatidia, and are one of the most advanced among insects. Each ommatidium contains 8 photoreceptor cells (R1-8), support cells, pigment cells, and a cornea. Wild-type flies have reddish pigment cells, which serve to absorb excess blue light so the fly isn’t blinded by ambient light.

Each photoreceptor cell consists of two main sections, the cell body and the rhabdomere. The cell body contains the nucleus while the 100-m-long rhabdomere is made up of toothbrush-like stacks of membrane called microvilli. Each microvillus is 12 m in length and ~60 nm in diameter. The membrane of the rhabdomere is packed with about 100 million rhodopsin molecules, the visual protein that absorbs light. The rest of the visual proteins are also tightly packed into the microvillar space, leaving little room for cytoplasm.

The photoreceptors in Drosophila express a variety of rhodopsin isoforms. The R1-R6 photoreceptor cells express Rhodopsin1 (Rh1) which absorbs blue light (480 nm). The R7 and R8 cells express a combination of either Rh3 or Rh4 which absorb UV light (345 nm and 375 nm), and Rh5 or Rh6 which absorb blue (437 nm) and green (508 nm) light respectively. Each rhodopsin molecule consists of an opsin protein covalently linked to a carotenoid chromophore, 11-cis-3-hydroxyretinal.

Expression of Rhodopsin1 (Rh1) in photoreceptors R1-R6

As in vertebrate vision, visual transduction in invertebrates occurs via a G protein-coupled pathway. However, in vertebrates the G protein is transducin, while the G protein in invertebrates is Gq (dgq in Drosophila). When rhodopsin (Rh) absorbs a photon of light its chromophore, 11-cis-3-hydroxyretinal, is isomerized to all-trans-3-hydroxyretinal. Rh undergoes a conformational change into its active form, metarhodopsin. Metarhodopsin activates Gq, which in turn activates a phospholipase C (PLC) known as NorpA.

PLC hydrolyzes phosphatidylinositol (4,5)-bisphosphate (PIP2), a phospholipid found in the cell membrane, into soluble inositol triphosphate (IP3) and diacylgycerol (DAG), which stays in the cell membrane. DAG or a derivative of DAG causes a calcium selective ion channel known as TRP (transient receptor potential) to open and calcium and sodium flows into the cell. IP3 is thought to bind to IP3 receptors in the subrhabdomeric cisternae, an extension of the endoplasmic reticulum, and cause release of calcium, but this process doesn’t seem to be essential for normal vision.

Calcium binds to proteins such as calmodulin (CaM) and an eye-specific protein kinase C (PKC) known as InaC. These proteins interact with other proteins and have been shown to be necessary for shut off of the light response. In addition, proteins called arrestins bind metarhodopsin and prevent it from activating more Gq. A sodium-calcium exchanger known as CalX pumps the calcium out of the cell. It uses the inward sodium gradient to export calcium at a stoichiometry of 3 Na+/ 1 Ca++.

TRP, InaC, and PLC form a signaling complex by binding a scaffolding protein called InaD. InaD contains five binding domains called PDZ domain proteins which specifically bind the C termini of target proteins. Disruption of the complex by mutations in either the PDZ domains or the target proteins reduces the efficiency of signaling. For example, disruption of the interaction between InaC, the protein kinase C, and InaD results in a delay in inactivation of the light response.

Unlike vertebrate metarhodopsin, invertebrate metarhodopsin can be converted back into rhodopsin by absorbing a photon of orange light (580 nm).

Approximately two-thirds of the Drosophila brain (about 200,000 neurons total) is dedicated to visual processing. Although the spatial resolution of their vision is significantly worse than that of humans, their temporal resolution is approximately ten times better.


The wings of a fly are capable of beating at up to 220 times per second. Flies fly via straight sequences of movement interspersed by rapid turns called saccades. During these turns, a fly is able to rotate 90 degrees in fewer than 50 milliseconds.

It was long thought that the characteristics of Drosophila flight were dominated by the viscosity of the air, rather than the inertia of the fly body. However, research in the lab of Michael Dickinson has indicated that flies perform banked turns, where the fly accelerates, slows down while turning, and accelerates again at the end of the turn. This indicates that inertia is the dominant force, as is the case with larger flying animals.. Recent work, however, has shown that while the viscous effects on the insect body during flight may be negligible, the aerodynamic forces on the wings themselves actually cause fruit flies’ turns to be damped viscously .

See also

Animal testing on invertebrates


^ Meigen JW (1830) (in German) (PDF). Systematische Beschreibung der bekannten europischen zweiflgeligen Insekten. (Volume 6). Schulz-Wundermann. 


^ a b Eric C. R. Reeve, ed (2001-06-23). “Drosophila melanogaster: The Fruit Fly”. Encyclopedia of genetics. USA: Fitzroy Dearborn Publishers, I. pp. 157. Retrieved 2009-07-01. 

^ “FlyBase: A database of Drosophila genes and genomes”. Genetics Society of America. 2009. Retrieved August 11, 2009. 

^ a b c d e f g Ashburner M, Thompson JN (1978). The laboratory culture of Drosophila. In: The genetics and biology of Drosophila. (Ashburner M, Wright TRF (eds.)). Academic Press. volume 2A: pp. 181. 

^ a b c d e f g Ashburner M, Golic KG, Hawley RS (2005). Drosophila: A Laboratory Handbook. (2nd ed.). Cold Spring Harbor Laboratory Press. pp. 1624. ISBN 0879697067. 

^ Bloomington Drosophila Stock Center at Indiana University: Basic Methods of Culturing Drosophila

^ a b Chiang HC, Hodson AC (1950). “An analytical study of population growth in Drosophila melanogaster”. Ecological Monographs 20 (3): 173206. doi:10.2307/1948580. 

^ Bakker K (1961). “An analysis of factors which determine success in competition for food among larvae of Drosophila melanogaster”. Archives Neerlandaises de Zoologie 14: 20081. 

^ Pitnick S (1996). “Investment in testes and the cost of making long sperm in Drosophila”. American Naturalist 148: 5780. doi:10.1086/285911. 

^ Gilbert SF (2006). “9: Fertilization in Drosophila”. Developmental Biology. Sinauer Associates. ISBN 978-0878932504. 

^ a b c d Price C et al (1999). “Sperm competition between Drosophila males involves both displacement and incapacitation”. Nature 400 (6743): 449452. doi:10.1038/22755. PMID 10440373. 

^ a b Pierce, Benjamin A. Genetics: A conceptual Approach. 2nd edition

^ a b Adams MD, Celniker SE, Holt RA, et al. (2000). “The genome sequence of Drosophila melanogaster”. Science 287 (5461): 218595. doi:10.1126/science.287.5461.2185. PMID 10731132. Retrieved 2007-05-25. 

^ Azpiazu N, Frasch M (1993). “tinman and bagpipe: two homeo box genes that determine cell fates in the dorsal mesoderm of Drosophila”. Genes and Development 7 (7b): 13251340. doi:10.1101/gad.7.7b.1341. PMID 8101173. 

^ Manning, Gerard (Oct 1, 2006). “Introduction to Drosophila”. The WWW Virtual Library: Drosophila. pp. 1. Retrieved 2009-08-17. 

^ Halligan DL, Keightley PD (2006). “Ubiquitous selective constraints in the Drosophila genome revealed by a genome-wide interspecies comparison”. Genome Research 16 (7): 87584. doi:10.1101/gr.5022906. PMID 16751341. 

^ Carvalho, AB (2002). “Origin and evolution of the Drosophila Y chromosome”. Current Opinion in Genetics & Development 12 (6852): 664668. doi:10.1016/S0959-437X(02)00356-8. 

^ Reiter, LT; Potocki, L; Chien, S; Gribskov, M; Bier, E (2001). “A systematic analysis of human disease-associated gene sequences in Drosophila melanogaster”. Genome Research 11 (6): 11141125. doi:10.1101/gr.169101. PMID 11381037. 

^ Bier lab (2008). “Homophila: Human disease to Drosophila disease database”. University of California, San Diego. Retrieved August 11, 2009. 

^ a b “Flymove”. Trends Genet. Trends Genet. 07.01.2009. pp. 1. Retrieved 2009-08-17. 

^ Hardie RC, Raghu P (2001). “Visual transduction in Drosophila”. Nature 413 (6852): 18693. doi:10.1038/35093002. PMID 11557987. 

^ Nichols R, Pak WL (1985). “Characterization of Drosophila melanogaster rhodopsin”. Journal of Biological Chemistry 260 (23): 126704. PMID 3930500. 

^ a b Raghu P, Colley NJ, Webel R, et al. (2000). “Normal phototransduction in Drosophila photoreceptors lacking an InsP(3) receptor gene”. Molecular and Cellular Neuroscience 15 (5): 42945. doi:10.1006/mcne.2000.0846. PMID 10833300. 

^ Wang T, Xu H, Oberwinkler J, Gu Y, Hardie R, Montell C, et al. (2005). “Light activation, adaptation, and cell survival Functions of the Na+/Ca2+ exchanger CalX”. Neuron 45 (3): 367378. doi:10.1016/j.neuron.2004.12.046. PMID 15694299. 

^ Rein, K. and Zockler, M. and Mader, M.T. and Grubel, C. and Heisenberg, M. (2002). “The Drosophila Standard Brain”. Current Biology 12 (3): 227231. doi:10.1016/S0960-9822(02)00656-5. PMID 11839276. 

^ Caltech Press Release 4/17/2003

^ S. Fry and M. Dickinson (2003). “The aerodynamics of free-flight maneuvers in Drosophila”. Science 300 (5618): 4958. doi:10.1126/science.1081944. PMID 12702878. 

^ T. Hesselberg and F.-O. Lehmann (2007). “Turning behaviour depends on frictional damping in the fruit fly “Drosophila””. The Journal of Experimental Biology 210: 431934. doi:10.1242/jeb.010389. 

Further reading

K. Haug-Collet, et al. (1999). “Cloning and characterization of a potassium-dependent sodium/calcium exchanger in Drosophila”. J. Cell Biol. 147 (3): 65970. doi:10.1083/jcb.147.3.659. PMID 10545508. 

R. Ranganathan, et al. (1995). “Signal transduction in Drosophila photoreceptors”. Annu. Rev. Neurosci. 18: 283317. doi:10.1146/ PMID 7605064. 

Adams MD, et al. (2000). “The genome sequence of Drosophila melanogaster”. Science 287 (5461): 218595. doi:10.1126/science.287.5461.2185. PMID 10731132. 

Kohler, Robert E. (1994). Lords of the Fly: Drosophila genetics and the experimental life. Chicago: University of Chicago Press. ISBN 0-226-45063-5. 

Popular media

“Inside the Fly Lab” – broadcast by WGBH and PBS, in the program series “Curious”, January 2008.

“How a Fly Detects Poison” – article describes how the fruit fly tastes a larvae-killing chemical in food.

External links

Wikispecies has information related to: Drosophila melanogaster

Wikimedia Commons has media related to: Drosophila melanogaster

A quick and simple introduction to Drosophila melanogaster

FlyBase – A Database of Drosophila Genes & Genomes

NCBI page on Drosophila melanogaster

The WWW Virtual Library: Drosophila

The Berkeley Drosophila Genome Project


The Interactive Fly A guide to Drosophila genes and their roles in development

Drosophila Nomenclature naming of genes

Make Your Own Fruit Fly Trap

Illustrates a simple to make non-toxic Vinegar fly trap

Measurement of Courtship Behavior in Drosophila melanogaster

Maintenance of a Drosophila Laboratory: General Procedures

Transcript In Situ Hybridization of Whole-Mount Embryos for Phenotype Analysis of RNAi-Treated Drosophila

Injection of dsRNA into Drosophila Embryos for RNA Interference (RNAi)

v  d  e

Major model organisms in genetics

Sheep   Lambda phage  E. coli   Chlamydomonas   Tetrahymena   Budding yeast  Fission yeast  Neurospora   Maize  Arabidopsis  Medicago truncatula  C. elegans   Drosophila   Xenopus  Zebrafish  Rat  Mouse

Categories: Drosophilidae | Model organisms | Sequenced genomes

Depression and Procrastination – The Terrible Duo Challenge

Virtually, people have at least dawdled with the procrastination process. Some even made it a way of life. Depression and procrastination appear to be a bothering phenomenon. The link between the two is connected and the lack of action simply correlates with one another.

In a broader view, procrastination and depression has been associated to several organizational and societal issues. Procrastinating is an inertial process where one subsequently do what one has done before and continues the pattern. Unless having the motivation to break from it, procrastination will devour ones self and eventually lead to a feeling of depression.

On the other hand, when one feels depressed, depression may overshadow all interests which leads to slow progression towards a goal. Depression is a common reaction to events that seem overwhelming or negative. The signs and symptoms of depression and the severity of the problem vary and the significance of the precipitating event.

So, the question now is “Which really comes first? Depression or procrastination?”

Some signs and symptoms of procrastination.

A lack of self-control is one bad habit to procrastinate. Finding oneself setting aside important tasks for an insignificant exciting activity might eventually lead to continuous practice on the inertial process.

Lack of organization wherein what needs to be done first would actually land to incomplete tasks. Less productivity may lead to lesser job contribution that would result to low effectivity.

Introducing negative ideas such as “I don’t want to. I couldn’t do it. I feel tired. I don’t feel like it. It’s too scary.” blunt exertions towards ones achievement.

Signs and symptoms of depression.

Emotional symptoms can include feelings of tiredness, sadness, emptiness, or numbness. Behavioral signs include irritability, inability to concentrate, difficulty making decisions, loss of sexual desire, crying, sleep disturbance, and social withdrawal. Physical signs of depression may include loss of appetite, weigh loss, constipation, headache, and dizziness.

Overcome procrastination.

The first thing to overcome this procrastinating process is to stop and address the problem right away! Consider intelligent ways to respond. If the problem is self-control, learn some disciplinary actions. Regulating this destructive habit is identifying the root cause issue. Practice some time management skills that would help find ways to reach ones goals and tame ones time.

Approach for depression.

Perhaps the best means in dealing with mild to moderate depression might be exercise, cognitive-behavioral therapy, organizing and focusing, and acceptance of the effects of depression suffered, which reduces how much one can accomplish.

Identifying Depression

Everyone knows what depression feels like. Everyone feels the blues at times. Sadness, discontent, and fatigue are natural parts of life. There is a relation between the blues and clinical depression, but the difference is like the difference between the sniffles and pneumonia.

Depressive disorders are whole person illnesses; they touch the body, feelings, thoughts, and behavior. The depression itself can make us feel as if it's of no use to search for help. The nice news is that 80 to 90 percent of people with depression can be treated successfully, but the bad news is that only one sufferer in three seeks treatment. More bad news is that not quite half the American public perceives depression as a character flaw, rather than an illness or emotional disorder. In addition, only half of all cases of depression are exactly diagnosed, and only half of those get adequate treatment.

We tend to muddle depression, sadness, and grief. But the opposite of depression is not happiness, but vitality – the power to experience a full range of emotion, including happiness, excitement, sadness, and grief. Depression is not an emotion itself. It's not sadness or grief, it's an illness. When we feel at our worst, sad, self-absorbed, and helpless, we are experiencing what people with depression experience, but they do not recover from those moods without help.

The trademark of depression is a insistent sad or empty mood, sometimes experienced as tension or anxiety. Life is with out pleasure. People with slight depressions may go through the motions of eating, sex, work, or play, but the activities seem like pointless; people with more severe depression withdraw from these activities, feeling too worn-out, tense, or hostile to take part. There is often a nagging fatigue, a sense of being incapable of focusing, a feeling of being inefficient.

People with depression generally feel a lowered self-esteem. In a depression, you may feel that you are a defenseless victim of fate, but also feel that you do not deserve any better. Feelings of guilt, shame, and hopelessness are common.

There are often a host of physical symptoms, of which sleep disturbances are key. People may have trouble falling asleep or may wake up early without feeling refreshed. Others may sleep excessively, again without feeling rested. Appetite may increase or decrease. There may be difficulty in sexual functioning. There may be harassing aches and pains that do not act in response to medical treatment. But there are physical illnesses that cause symptoms like depression – Lyme depression, diabetes, thyroid conditions, anemia – and depressions can cause physical symptoms like other diseases.

If you are feeling depressed, it is important to be sure that an underlying health problem does not exist, and you should see your physician for a checkup. At the same time, if you know you have a health problem and are feeling depressed, do not presume you will feel better once the health problem is under control.

There is a sequential process in the recognition of depression. First is a stage of confused pain in which the sufferer knows he suffers, but does not know why. People often blame circumstances. Adolescents blame their home lives, married people blame their spouses, and employees blame their bosses. But there is recognition that the pain is not ordinary.

The second stage is recognition that something is definatley amiss. It may be that external circumstances have changed but the pain is on going, or it may be a slow recognition that the suffering is so dangerous that circumstances can not be blamed. This is a painful recognition that often takes years. It is an acknowledgment of a damaged self. But because of the nature of depression, the self-blame and guilt that are manifestations of the disease, this acceptance does not always lead to seeking help.

People then may move to the third stage, a crisis that frequently leads to professional intervention and diagnosis. It is often a suicide attempt or psychiatric hospitalization. The diagnosis often provides hope, that treatment or a cure is possible, and explanation, a way to understand what has only been confusion before. The fact is that this is a diagnosis of a mental illness, with all the shame and stigma that that entails.

The fourth stage involves acceptance of an illness identity. Depression comes to be seen as an outside agent invading the self, rather than as a manifestation of the self.

It is essential that anyone suffering from depression gets good help from a competent, qualified professional. If the warning signs are clear, always seek a professional diagnosis. Going to a health professional with your problems could prove, at worse, embarrassing, if the problem is really just a seasonal case of the blues that can be treated with without medical intervention, but the potential cost of failing to diagnose a serious case of depression should far outweigh any concern about conceivable embarrassment.

An Introduction to Driving Phobias

For some people, seatbelts, airbags and GPS navigators just aren’t enough. The thought of driving alone is enough to send serious shivers up their spines.

Decades after Henry Ford revolutionized the automobile industry, choking up city streets and freeways with high-volume vehicular traffic, people have started to develop fears of these horseless carriages. Yes, there is such a thing as driving phobia – phobias, in fact.

But first, what is a phobia? Psychologists define it as an uncontrollable or irrational fear of a certain object, person, or particular situation.

When you feel scared whenever you get on a train or a bus, you may be suffering from traveling phobia. When the thought of maneuvering a vehicle through traffic leaves you breathless, that’s more likely driving phobia.

If you break into sweat while driving your boss’s beloved Bugati, which he asked you to take to the car wash (or what do the call it these days, car spa?), well, it’s not really a phobia. It just shows how you love your career.

Usually, a phobia is easily determined by just observing its symptoms, such as the feeling of breathlessness, excessive sweating, trembling, nausea, and most of all, having palpitations. These indications of panic usually have mental causes but the effects are more obvious.

It is often regarded as a manifestation of an obsessive-compulsive disorder (OCD), which usually leaves a person feeling anxious in almost all cases, especially when he gets near the object of fear.

Learning how to drive is becoming a necessity. It has become as important as knowing how to swim. The reasons vary. Some people just love driving fancy cars, while others really enjoy the mobility the skill offers. You’re missing out on a lot of things, therefore, if you’re afraid of taking the steering wheel.

As said earlier there are several driving phobias, as we have unique experiences with the automobile. People may have any or most of these fears: driving in an unfamiliar place, on motorways, in dual carriageways, getting caught in heavy traffic, getting through narrow lanes, driving in certain weather conditions, etc.

Perhaps the most common driving phobias are fear of turning left at an intersection (left-lane-drive countries like the United Kingdom will have no problem with this, of course) and driving through snowy weather, especially at night.

Don’t feel weird about yourself, however. You’re not headed for the loony bin. In fact, it is estimated that 10 percent of the world’s total population is suffering from different phobias.

So at this point, start teaching yourself not just the lessons of safe driving but also of managing your fears until you finally overcome your driving phobia. No method is effective if you yourself don’t think positively. This might sound difficult for you, but undergoing through some mental and behavioral changes comprise your basic steps.

Common examples of these changes include having the positive affirmation especially when it comes to your thought processing. Driving isn’t a difficult task when you know how, and you won’t easily get that driving license if you don’t really qualify.

However, there are some cases in which the degree of fear has gone beyond ordinary. So if you can’t find the solutions in your end, find it somewhere else. Sites like phobias-help and anxiety-panic reviews are a great help, or just see a psychiatrist for therapy and medication.

Itchy Scalp and Anxiety? – How to Combat Itchy Scalp and Anxiety

An itchy scalp and anxiety have more in common than you may think. Can anxiety or stress really cause a sore and painful scalp? The answer to that is yes, anxiety has been proven to cause scalp irritation. Whether it’s financial stress, stress related to work, taking care of the children, hormonal and pregnancy issues or menopause, there is a direct link between an itchy scalp and anxiety, and these daily stresses can have a serious impact on the condition of your scalp. So stress really does go straight to your head!

In most cases, simple lifestyle changes are more beneficial than a change of products or remedies. People that suffer with an itchy scalp and anxiety need to balance their stress levels. Now, while this may sound easier said than done, there are always small changes you can make to relieve the stress in your life, and certain remedies will help in the soothing of an irritated scalp. Talking through your problems with a friend or partner, can often be very beneficial in finding a way to begin to reduce and relieve your anxiety levels and avoid the problem of an itchy scalp.

To balance stress levels you need to have a source of relaxation. Yoga is a great way to just relax for thirty minutes everyday. There are many forms of yoga that fulfill different needs and wants. Breathing techniques, poses and exercises associated with yoga are known to improve management and relaxation skills. Yes, relaxation is a skill that not many people possess nowadays. There are yoga classes everywhere from big cities to small towns. If you are more interested in relaxing with yoga in the comfort of your own home, then consider doing some research on the topic online or in your local library.

Aromatherapy is an alternate form of health practice that uses essential oils to stimulate our bodies senses. These essential oils are extracts from aromatic plants that are mixed with a carrier oil to produce a calming effect on both the mind and the body. Aromatherapy is great for relaxation, particularly after a hard day.

So whether yoga or aromatherapy suits you best, it is important to try and relax to cure your itchy scalp and anxiety. The stresses of life take everything out of us and it is essential to give some of it back by relaxing.

For an immediate temporary soother for your itchy scalp, try the following natural remedy:

Get three sprigs of Rosemary.

Chop them up and add it to three bags of Chamomile tea.

Boil the mixture gently, let it cool, strain it and rinse your hair with this liquid for a calming anti-inflammatory effect on your itchy scalp.

Nerve Entrapment Syndromes and Massage Therapy

In my San Antonio, Texas based Massage Therapy and Bodywork practice I often treat men and women who are experiencing pain from various nerve entrapment syndromes. Like many painful conditions involving the body’s soft tissues, nerve entrapment syndromes respond quite well to massage therapy and bodywork.

What Are Nerve Entrapment Syndromes?

Nerve Entrapment Syndromes are nerve impingement conditions in which nerves or nerve roots are placed under abnormal pressure by soft tissues such as muscles, tendons, ligaments, or fascia. The abnormal pressure on the nerves or nerve roots creates pain locally or radiating outward, numbness or tingling in the area supplied by the nerve and possibly weakness or twitching of affected muscles. Nerve entrapment syndromes are fairly common and you may have heard of some of them like Carpal Tunnel Syndrome, Piriformis Syndrome, Thoracic Outlet Syndrome, Meralgia Paresthetica, Tarsal Tunnel Syndrome, and Cubital Tunnel Syndrome.

What Are The Causes Of Nerve Entrapment Syndromes?

There are a number of causes for Nerve Entrapment Syndromes. Direct trauma to the muscles or tendons are a common cause and this includes injuries which quickly overstretch and damage soft tissues like whiplash does. Overworking muscles and tendons through excessive exercise, or through incorrect repetitive motions (Repetitive Stress Injuries) including typing and assembly line work can cause several Nerve Entrapment Syndromes. Additionally, postural distortions such as Forward Head Posture, Leg Length Discrepancy, or Lower Crossed Syndrome often lead to entrapment conditions. In rare cases certain genetic factors can lead to Nerve Entrapment Syndromes.

Massage Therapy And Bodywork For Nerve Entrapment Syndromes

There are many ways that massage therapy and bodywork can be used to treat Nerve Entrapment Syndromes. The massage therapist will employ a number of techniques to relieve these conditions. For example the massage therapist may use Neuromuscular Therapy or Trigger Point Therapy to eliminate myofascial trigger points in the muscles entrapping the affected nerve. The massage therapist could also use Myofascial Release techniques or Deep Tissue Massage techniques to release adhesions between the muscles and surrounding ligamentous and fascial tissues while also using Muscle Energy Techniques to gently lengthen the affected muscles. Nerve Entrapment Syndromes also respond well to positional release therapies such as Ortho-Bionomy which work with the body’s nervous system to release muscles and improve joint movement in the area. In addition to working on the muscles entrapping a nerve or nerve root it may be necessary to provide therapy for other muscles and soft tissues nearby and even to opposing muscles to improve muscular balance. Comprehensive treatment with massage and bodywork, in conjunction with a home program of stretching and exercise, usually helps to completely resolve Nerve Entrapment Syndromes.

Other Treatments For Nerve Entrapment Syndromes

While massage therapy and bodywork are an excellent treatment for Nerve Entrapment Syndromes, the serious nature of these conditions means that there are other additional treatments you should discuss with your physician:

Anti-inflammatory medications
Muscle Relaxer medications
Anesthetic and Steroid Injections

Other Names For Nerve Entrapment Syndromes

Pinched Nerve
Nerve Entrapment Neuropathy

The information in this article has been provided for information purposes only. It is not meant to provide a medical diagnosis, only a licensed physician may diagnose Nerve Entrapment Syndromes. If you feel that you have the symptoms of a Nerve Entrapment Syndrome please see your physician for a proper diagnosis and plan of treatment which may include massage therapy and bodywork. There are a number of more serious conditions that resemble Nerve Entrapment Syndromes that could require immediate medical attention.

If, after consulting your physician, you would like to pursue treatment of your particular Nerve Entrapment Syndrome with Massage Therapy and Bodywork please contact me at my San Antonio Massage and Bodywork practice or contact a Massage Therapist near you.

Anxiety Sleeping Disorders – Insomnia

Anxiety sleeping disorders are extremely stressful and lead to a terrible kind of unhealthiness. Too many have suffered from anxiety induced sleeping disorders. Sufferers that grapple with this little slice of hell have an insurmountable difficulty in achieving sleep, primarily as a result of the constant ongoing mental chatter. Fears, phobias, or stress-packed worries – particularly those that are work related (project deadlines, business meetings, tasks delegated to lower staff, etc.), worries about bills and accounts, and etc. can cause an endless whipping tornado of stressful anxiety that just continuously feeds into our sleeping disorders.

If a sufferer of anxiety induced sleeping disorders can finally beyond the chaotic worry, break the cycle of ceaseless thoughts and actually get some rest, the experienced short sleep is often fraught with disturbing nightmares and tossing and turning in bed throughout the entire session of sleep. This inevitably leads to experiencing a more fatigued state upon awaking in the morning than the sleeper was the evening before. The effects of anxiety sleeping disorders eventually causes the immune system to weaken and break down, as our bodies become deprived of the much needed sleep used to rejuvenate and recharge becomes more and more nonexistent.

Anxiety causing sleeping disorders creates a kind of double-fisted attack on the immune system, the body and the brain, as sleep deprivation eventually affects our sense of better judgment, our cognitive thinking abilities, higher sense of reasoning and even moral strength. Wrestling with anxiety feeds into sleeping disorders, but ironically, it also depletes us of our energy at the same time, leaving us drained and even more exhausted. This type of physical and mental anguish leads to serious sickness and after extended lengths of time can even also cause serious damage to the brain in the more severe cases. Those who suffer from anxiety sleeping disorders can only find absolute relief by means of one special type of therapy – a good night's restful sleep.

Main Characteristics of Streptococcus Infections

Symptoms of sore throats caused by streptococcus bacteria group A differ from easy headaches and fever to severe pain and inflammations of throat and tonsils. In any form of apparition, the streptococcus infection must be treated with antibiotics to prevent complications and contagiousness for other persons.

In spite of the cases when the streptococcus is detected in rapid tests, most of the sore throats are triggered by viral infections, most of them caused by Influenza viruses. There are more types of streptococci responsible for different cases of throat pains; some of the strains release dangerous toxins that trigger allergic reactions such as fever rashes. Left untreated, streptococcus infections can spread to the other main organs and cause conditions affecting the heart like rheumatism or the kidneys like the glomerulonephritis.

Children under the age of three rarely develop streptococcus infections and most of the cases do not originate in the throat. The most exposed patients to sore throats triggered by the strep bacteria are children between 5 and 15 years of age. Most often, streptococcus infections occur during the months when children are in close contact with each other, representing late fall, winter and early spring.

The streptococcus sore throat develops the first symptoms within the first 3-5 days after they have been exposed and have caught the bacteria. This is the incubation period required for streptococci to multiply inside the body. Symptoms like fever, sore throat, headaches, chills, stomachaches and nausea appear sudden. The sore throat appears inflamed, irritated and the tonsils are red, swollen and covered with white or yellow points on the surface. On the roof of the mouth, some patients develop red or purple spots. The lymph nodes around the neck usually appear inflamed due to the bacterial aggression.

From persons to person, the sore throat symptoms differ from very mild forms to severe pain and general illness.

Streptococcus infections causing sore throat can easily be misdiagnosed as they resemble very much to other types of conditions triggered by Adenoviruses, Epstein Barr virus or by the bacteria Mycoplasma. Therefore, a complete diagnosis can only be established after a rapid strep test, a physical examination and a medical history of the patient. An appropriate medication with antibiotics can be prescribed when the positive diagnose of streptococcus is confirmed with a bacterial culture.

The classic treatment for streptococcus infections is represented by antibiotics that cannot reduce the disease period very much but can prevent complications and prevent the patients from spreading the bacteria. Antibiotics are only recommended if the exact type of streptococcus or other microbe has been established. The antibiotic effect can be increased by the administration of Ibuprofen.

Patients diagnosed with streptococcus must be kept in quarantine, especially children, in order to prevent contact with healthy subjects. After the antibiotic therapy has been started, persons can resume their activity inside the community. All patients should change their toothbrush after they gave been treated from streptococcus in order to prevent re-infection.

For more resources on different strep throat subjects check out this link You can find great content regarding strep throat in adults, strep throat symptoms, home remedy for strep throat

Nail Fungus – Symptoms and Treatments for Nail Fungal Infection

Having a nail fungal infection is really annoying. Where did it come from? Well, you probably wear your shoes too much or you were walking barefoot in a public swimming pool or are being negligent in using communal comfort rooms. Maybe you haven’t heard of nail fungi and didn’t care until you found them occupying 10 per cent of your feet. It nailed it! Now read this for your awareness:

Nail fungi, onychomycosis (on-i-ko-mi-ko-sis) or tinea unguium in scientific terms, commonly infects the feet because these minuscule fiends love dark and humid spots of the human body. Since our feet spend most of their waking time enfolded in leathers or rubbers and inefficient socks, the fungi often breed in the toenails where there is enough warmth and moisture.

Beware! This kind of fungus is naturally anaerobic. It means that they indulge in environment with less supply of oxygen. It belongs to the dermatophytes family, which also causes athlete’s foot, ringworm, psoriasis, and jock itch among others. Some of the sources of these fungi are yeasts and molds. They thrive in soggy areas and can penetrate our nails through contact with an infected nail or improper hygiene.

At first, the fungus is just a white or yellowish spot under the nail. It then chomps through the keratin compound of the nails and spreads. Soon, you will feel pain while your nail gets brittle and thick with the ugly discoloration. In some cases, the infected area bleeds and develops a gooey discharge.

If you are not diabetic, you’re lucky. People with diabetes could hardly treat nail fungi when infected due to weak immune system and blood circulation conditions. A mild infection leads to greater damage on the course. This is the case also for persons with leukemia.

Normally, nail fungal infection is cured by proper hygiene and medication. Topical and oral treatments are taken in or applied as prescribed by doctors. Antifungal brands can be had over-the-counter such as Lamisil, Tinactin, Penlac, and the like. The medication may take three months or more until a new nail sprouts. However, this does not guarantee your nails to be fungi-free forever. They sometimes recur if triggered.

To prevent nail fungus, you must follow the basic rules in hand and foot hygiene. Keeping your nails dry and clean saves you in the long run. And choose the right socks to wear! Synthetic socks perform better in terms of dryness than cotton-made. Plus, don’t stock your feet too long inside your shoes. Give them short breaks during daytime to keep it ventilated. Foot powder is highly recommended, too. The fingernails rarely acquire nail fungi but to be sure, avoid overexposing it to water or chemicals. If you have to, always

dry them thoroughly.

Nail polish and artificial nails may be cute but don’t fancy them too much. Use them only occasionally. As a rule, be careful with the instruments of your favorite salon. Make sure they are sterilized because Fungi are highly contagious.

Your nails deserve the right kind of pampering. Take good care of it before it’s too late.

Ankle Sprains & Balance Training

Ankle sprains are a common athletic injury. Previous ankle sprains and a high body mass index (BMI) have been identified as risk factors for non-contact inversion ankle sprains (NCIAS) in football players, regardless of position. Commonly, ankle braces or tape are used in an attempt to reduce the risk of sprain, but the effectiveness of these strategies has recently been called into question. However, there is increasing support for the use of single limb balance training (SLBT) to reduce ankle injury risk.

The authors of this study hypothesized that having previous ankle injury and a high BMI increase NCIAS risk due to impaired ankle stability, and a lack of control of upper body mass during the dynamic movements required in football. As such, SLBT could counteract these deficits and lower risk. Therefore, this study aimed to determine if SLBT on a foam stability pad can reduce NCIAS incidence in high school football players who were at increased risk.

During the intervention period, 125 different players from 2 high school football teams were observed over 3 seasons. A previous history of ankle sprains, height, body mass, and use of ankle braces or tape were noted. 175 player seasons were followed in total. Players were assigned risk levels (minimal, low, moderate, or high) for NCIAS based on their BMI and previous ankle injury history. Players in the low, moderate, or high risk categories were assigned to perform the stability pad intervention.

Subjects in the intervention group performed SLBT on a foam stability pad for 5 minutes per leg (both legs were trained), five times per week for 4 weeks in the preseason. Subjects completed the same type of training twice weekly for nine weeks during football season. The SLBT was incorporated into the subjects' regular weight room routines as part of a balance training station. Compliance was monitored by the team Athletic Therapist, and subjects had to make up for missed sessions.

The main outcome measure was incidence of NCIAS, which was defined as a sprain that required the player to miss at least one game or practice, and it had to be non-contact (ie did not occur while tackling or blocking, etc). The team Athletic Therapist collected data on NCIAS injuries and the number of missed games and practices due to such an injury. Injury incidence was calculated in units of per 1000 player exposures (an exposure being participation in a game or practice, and the analysis included the use of 95% confidence intervals). Statistical analysis included chi square and Fisher exact tests to compare NCIAS incidence before and after the introduction of the intervention. 107 player seasons (for 84 players) were followed prior to the introduction of the intervention as a comparison.

Pertinent results of this study include:

• 128 out of the 175 players seasons were classified as low, moderate, or high risk and were thus assigned to the intervention analysis
• 12 players were non-compliant, the rest of the players completed at least 34 out of 38 training sessions (20 preseason and 18 in-season)

• pre-intervention period: the prevalence of NCIAS was 3% in the minimal risk group and 18% in the low-moderate-high risk group; 21 of the 84 players sustained an inversion ankle sprain, 13 of which were NCIAS; nine of those were by players with a previous history of ankle sprain
• post-intervention period: the prevalence of NCIAS was 7% prevalence in the minimal risk group and 5% prevalence in the low-moderate-high risk group (actually 4% as one of the players in this group did not complete the intervention / was non-compliant); 20 out of 125 players had inversion ankle injuries, 9 of which were NCIAS and five of those were by players with a previous history of ankle sprain
• overall, the prevalence of NCIAS was significantly reduced for those at risk – a 77% reduction in injury incidence for those in similar risk groups (2.2 / 1000 exposures to 0.5 / 1000 in the groups when combined).

Dog Coughing – Five Common Causes of Canine Coughing

Dog coughing can occur for many different reasons, some of them serious and others minor. Your dog can cough if he drinks water too fast, or he can cough due to lung or heart conditions. Other common causes include parasites, allergies, and distemper. This article will take a look at some of the common causes of canine coughing.

Kennel Cough

As it’s name suggests, the main symptom of this disease is frequent coughing. Dogs with a healthy immune system can get over it in roughly two weeks. However, puppies and smaller breeds may develop thick secretions that can cause pneumonia. This can be a life-threatening condition.


One of the next common causes of dog coughing is distemper. Most canines are vaccinated from this disease, but all of them aren’t. This disease can be fatal to puppies and dogs without a healthy immune system. Distemper causes symptoms that mimic a human’s head cold. They include a dry cough, yellow discharge from eyes and nose, and a relatively high fever.


Roundworms are internal parasites that can also cause canine coughing. After infecting your dog, they wind up living in his intestine. Dogs because infected by ingesting soil that has been contaminated with eggs. Once the eggs hatch, the worms crawl up your dog’s windpipe which results in coughing. A light infestation of roundworms is easily treatable.


Heartworms on the other hand present a much more serious problem. An infestation of these worms is often fatal. By the time your dog starts to cough, the disease has already progressed to an advanced stage. Treatment involves a series of injections given weeks apart. The first injection contains arsenic which will kill the worms. The next injection is aimed at destroying microfilariae circulating in the blood.


Infectious tonsillitis is a condition in which your dog’s tonsils become swollen and painful. These two symptoms prompt your dog to try to cough the tonsils up violently. Some dogs will also paw at their mouths. Treatment usually involves giving your dog antibiotics for a few weeks until the infection is cleared up.