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Immunomodulating effect of autohaemotherapy (a literature review). PMID 3534085 [PubMed indexed for MEDLINE]

J Hyg Epidemiol Microbiol Immunol. 1986;30(3):331-6.

Immunomodulating effect of autohaemotherapy (a literature review).
Klemparskaya NN, Shalnova GA, Ulanova AM, Kuzmina TD, Chuhrov AD.

Abstract
An analysis is presented of experimental and clinical data from different authors on the stimulating effect of autohaemotherapy with regard to the immunological reactivity of humans and animals as well as in vitro experiments with lymphocytes. Erythrolysate has been found to exert a more powerful effect than intact erythrocytes. The stimulating effect of autohaemotherapy on both irradiated and non-irradiated animals manifests itself in an increase in resistance to infection (increased LD50 in experimental infection), enhanced production of antibodies to microbial and tissue antigens and activated functioning of cell-mediated immune defence mechanisms. The favourable influences on radioresistance and the antitumour effect of authohaemotherapy are described. Induced desensitization plays an important part in the mechanism of action of autohaemotherapy. The administration of large doses of erythrocytes or of erythrolysate results in immunosuppression. Autohaemotherapy does not cause side effects and is feasible both on an in-and out-patient basis.

PMID: 3534085

[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/3534085

Autohemotherapy: an immunization with our own blood

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Mal Di Stomaco Rimedi, Bruciore All Esofago, Come Combattere L Acidita Di Stomaco

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Le cause del reflusso acido

La sindrome da reflusso acido, nota anche come sindrome da reflusso gastro-esofageo (GERD), si verifica a causa della coesistenza di diversi disturbi medici e di stile di vita.

Fattori fisiologici che scatenano GERD includono l'ipotonia dello sfintere esofageo inferiore (LES) (il graduale indebolimento del LES), insieme con il flusso retrogrado del contenuto dello stomaco nell'esofago, e il livello di sensibilità del muco esofagea al contenuto riflusso.


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The term subclavian steal describes retrograde blood flow in the vertebral artery associated with proximal ipsilateral subclavian artery stenosis or occlusion, usually in the setting of subclavian artery occlusion or stenosis proximal to the origin of the vertebral artery. Alternatively, innominate artery disease has also been associated with retrograde flow in the ipsilateral vertebral artery, particularly where the subclavian artery origin is involved. Subclavian steal is frequently asymptomatic and may be discovered incidentally on ultrasound or angiographic examination for other indications, or it may be prompted by a clinical examination finding of reduced unilateral upper limb pulse or blood pressure. In some cases, patients may develop upper limb ischemic symptoms due to reduced arterial flow in the setting of subclavian artery occlusion, or they may develop neurologic symptoms due to posterior circulation ischemia associated with exercise of the ipsilateral arm.[1] Treatment has traditionally consisted of open subclavian artery revascularization, typically via carotid-subclavian bypass or subclavian artery transposition, which are generally durable procedures. Newer, less invasive options include endovascular intervention with recanalization as appropriate and angioplasty and stenting if required. The clinical relevance of subclavian steal was described in 1961 by Reivich, Holling and Roberts; however, the recognition of retrograde vertebral artery flow dates back another 100 years to Harrison and Smyth. Some papers, including a previous version of this article, advocate restricting the term subclavian steal to patients with neurologic symptoms only, but this is incorrect in view of the substantial literature using this term to describe the hemodynamic scenario of retrograde vertebral flow and proximal subclavian artery disease.

Multiple sclerosis (MS) affects the brain and spinal cord. Early MS symptoms include weakness, tingling, numbness, and blurred vision. Other signs are muscle stiffness, thinking problems, and urinary problems. Treatment can relieve MS symptoms and delay disease progression.

Sickle cell anemia is an inherited form of anemia — a condition in which there aren't enough healthy red blood cells to carry adequate oxygen throughout your body. Normally, your red blood cells are flexible and round, moving easily through your blood vessels. In sickle cell anemia, the red blood cells become rigid and sticky and are shaped like sickles or crescent moons. These irregularly shaped cells can get stuck in small blood vessels, which can slow or block blood flow and oxygen to parts of the body. There's no cure for most people with sickle cell anemia. However, treatments can relieve pain and help prevent further problems associated with sickle cell anemia.

Primary infection with herpes simplex viruses (HSVs) is clinically more severe than recurrent outbreaks. However, most primary HSV-1 and HSV-2 infections are subclinical and may never be clinically diagnosed. Orolabial herpes Herpes labialis (eg, cold sores, fever blisters) is most commonly associated with HSV-1 infection. Oral lesions caused by HSV-2 have been identified, usually secondary to orogenital contact. Primary HSV-1 infection often occurs in childhood and is usually asymptomatic. Primary infection Symptoms of primary herpes labialis may include a prodrome of fever, followed by a sore throat and mouth and submandibular or cervical lymphadenopathy. In children, gingivostomatitis and odynophagia are also observed. Painful vesicles develop on the lips, the gingiva, the palate, or the tongue and are often associated with erythema and edema. The lesions ulcerate and heal within 2-3 weeks. Recurrences The disease remains dormant for a variable amount of time. HSV-1 reactivation in the trigeminal sensory ganglia leads to recurrences in the face and the oral, labial, and ocular mucosae. Pain, burning, itching, or paresthesia usually precedes recurrent vesicular lesions that eventually ulcerate or form a crust. The lesions most commonly occur in the vermillion border, and symptoms of untreated recurrences last approximately 1 week. Recurrent erythema multiforme lesions have been associated with orolabial HSV-1 recurrences. A recent study reported that HSV-1 viral shedding had a median duration of 48-60 hours from the onset of herpes labialis symptoms. They did not detect any virus beyond 96 hours of symptom onset.[7] Genital herpes HSV-2 is identified as the most common cause of herpes genitalis. However, HSV-1 has been increasingly identified as the causative agent in as many as 30% of cases of primary genital herpes infections likely secondary to orogenital contact. Recurrent genital herpes infections are almost exclusively caused by HSV-2. Primary infection Primary herpes genitalis occurs within 2 days to 2 weeks after exposure to the virus and has the most severe clinical manifestations. Symptoms of the primary episode typically last 2-3 weeks. In men, painful, erythematous, vesicular lesions that ulcerate most commonly occur on the penis, but they can also occur on the anus and the perineum. In women, primary herpes genitalis presents as vesicular/ulcerated lesions on the cervix and as painful vesicles on the external genitalia bilaterally. They can also occur on the vagina, the perineum, the buttocks, and, at times, the legs in a sacral nerve distribution. Associated symptoms include fever, malaise, edema, inguinal lymphadenopathy, dysuria, and vaginal or penile discharge. Females may also have lumbosacral radiculopathy, and as many as 25% of women with primary HSV-2 infections may have associated aseptic meningitis. Recurrences After primary infection, the virus may be latent for months to years until a recurrence is triggered. Reactivation of HSV-2 in the lumbosacral ganglia leads to recurrences below the waist. Recurrent clinical outbreaks are milder and often preceded by a prodrome of pain, itching, tingling, burning, or paresthesia. Individuals who are exposed to HSV and have asymptomatic primary infections may experience an initial clinical episode of genital herpes months to years after becoming infected. Such an episode is not as severe as a true primary outbreak. More than one half of individuals who are HSV-2 seropositive do not experience clinically apparent outbreaks. However, these individuals still have episodes of viral shedding and can transmit the virus to their sexual partners. Other HSV infections Localized or disseminated eczema herpeticum is also known as Kaposi varicelliform eruption. Caused by HSV-1, eczema herpeticum is a variant of HSV infection that commonly develops in patients with atopic dermatitis, burns, or other inflammatory skin conditions. Children are most commonly affected. Herpes whitlow, vesicular outbreaks on the hands and the digits, was most commonly due to infection with HSV-1. It usually occurred in children who sucked their thumbs and, prior to the widespread use of gloves, in dental and medical health care workers. The occurrence of herpes whitlow due to HSV-2 is increasingly recognized, probably due to digital-genital contact. Herpes gladiatorum is caused by HSV-1 and is seen as papular or vesicular eruptions on the face, arms, or torsos of athletes in sports involving close physical contact (classically wrestling). Disseminated HSV infection can occur in females who are pregnant and in individuals who are immunocompromised. These patients may present with atypical signs and symptoms of HSV, and the condition may be difficult to diagnose. Herpetic sycosis, a follicular infection with HSV, may present as a vesiculopustular eruption on the beard area. This infection often results from autoinoculation after shaving through a recurrent herpetic outbreak. Classically caused by HSV-1, there have been rare reports of relapsing beard folliculitis caused by type 2 HSV.[8] Neonatal HSV HSV-2 infection in pregnancy can have devastating effects on the fetus. Neonatal HSV usually manifests within the first 2 weeks of life and clinically ranges from localized skin, mucosal, or eye infections to encephalitis, pneumonitis, disseminated infection, and demise. Most women who deliver infants with neonatal HSV had no prior history, signs, or symptoms of HSV infection. Risk of transmission is highest in pregnant women who are seronegative for both HSV-1 and HSV-2 and acquire a new HSV infection in the third trimester of pregnancy. Factors that increase the risk of transmission from mother to baby include the type of genital infection at the time of delivery (higher risk with active primary infection), active lesions, prolonged rupture of membranes, vaginal delivery, and an absence of transplacental antibodies. The mortality rate for neonates is extremely high (>80%) if untreated.

Atopic dermatitis (eczema) is a condition that makes your skin red and itchy. It's common in children but can occur at any age. Atopic dermatitis is long lasting (chronic) and tends to flare periodically and then subside. It may be accompanied by asthma or hay fever.

The virus was first discovered in 1964 when Sir Michael Anthony Epstein and Ms. Yvonne Barr found it in a Burkitt lymphoma cell line. In 1968, the virus was linked to the disease infectious mononucleosis. Infection with Epstein-Barr virus (EBV) is common and usually occurs in childhood or early adulthood. EBV is the cause of infectious mononucleosis (also termed "mono"), an illness associated with fever, sore throat, swollen lymph nodes in the neck, and sometimes an enlarged spleen. It is also known as human herpes virus 4. Although EBV can cause mononucleosis, not everyone infected with the virus will get mononucleosis. Less commonly, EBV can cause more serious disease. Symptoms caused by EBV are usually mild and self-limited, but the virus persists in the body for life. It can be reactivated quietly without causing symptoms and may contaminate saliva. Thus, otherwise healthy people can spread the virus to uninfected people through kissing or sharing

There are two main types of influenza (flu) virus: Types A and B. The influenza A and B viruses that routinely spread in people (human influenza viruses) are responsible for seasonal flu epidemics each year. Influenza A viruses can be broken down into sub-types depending on the genes that make up the surface proteins. Over the course of a flu season, different types (A & B) and subtypes (influenza A) of influenza circulate and cause illness.

The difference between bronchitis and pneumonia is that bronchitis causes an inflammation of the air passages while pneumonia causes fluid in the lungs due to an infection. The common cold however, allows people to remain active and presents itself with a clear runny nose, cough, and a low-grade or no fever.