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If you look at someone’s back, you’ll see that the spine runs straight down the middle. When a person has scoliosis, their backbone curves to the side. The angle of the curve may be small, large or somewhere in between. But anything that measures more than 10 degrees is considered scoliosis. Doctors may use the letters “C” and “S” to describe the curve of the backbone. You probably don’t look directly at too many spines, but what you might notice about someone with scoliosis is the way they stand. They may lean a little or have shoulders or hips that look uneven. What Causes Scoliosis? In as many as 80% of cases, doctors don’t find the exact reason for a curved spine. Scoliosis without a known cause is what doctors call “idiopathic.” Some kinds of scoliosis do have clear causes. Doctors divide those curves into two types -- structural and nonstructural. In nonstructural scoliosis, the spine works normally, but looks curved. Why does this happen? There are a number of reasons, such as one leg’s being longer than the other, muscle spasms, and inflammations like appendicitis. When these problems are treated, this type of scoliosis often goes away. In structural scoliosis, the curve of the spine is rigid and can’t be reversed
The hepatitis E virus, responsible for major epidemics of viral hepatitis in subtropical and tropical countries, was cloned only 7 years ago.1 Hepatitis E was found to belong to the family of Caliciviridae, which includes the Norwalk virus—a common cause of gastroenteritis in humans—and consists of a single, plus-strand RNA genome of approximately 7.2 kb without an envelope (Fig. 1). The virus contains at least three open reading frames encoding viral proteins against which antibodies are made on exposure. These antibodies, especially those against the capsid protein derived from the second open reading frame2 and a protein of unknown function derived from the third open reading frame, are detected by currently available serologic assays. Retrospective studies on stored sera of past epidemics of viral hepatitis in Mexico, Africa, Afghanistan, Pakistan, India, Bangladesh, Burma, Nepal, and Borneo have revealed that all were caused by strains of hepatitis E. In addition, hepatitis E was found to be responsible for the hepatitis epidemic in the southern part of Xinjiang, China, in which 120,000 persons became infected between September 1986 and April 1988.3 Hepatitis E predominantly affects young adults (15 to 40 years old). The symptoms of hepatitis E are similar to those of hepatitis A. Frequently, a prodrome consisting of anorexia, nausea, low-grade fever, and right upper abdominal pain is present 3 to 7 days before jaundice develops. Aminotransferase levels peak (usually between 1,000 and 2,000 U/L) near the onset of symptoms; bilirubin levels (10 to 20 mg/dL) peak later. Jaundice usually resolves after 1 to 2 weeks. In about 10% of cases, the disease is fulminant—especially in pregnant women, among whom mortality rates as high as 20% due to hemorrhagic and thrombotic complications have been reported. No evidence has suggested that hepatitis E can cause chronic infection. Transmission is by the fecal-oral route, predominantly through fecally contaminated drinking water supplies. In addition, however, preliminary reports have suggested transmission of the hepatitis E virus through blood transfusions. Volunteer studies confirmed the presence of the virus in serum and feces before and during clinical disease.4 The virus is shed into feces approximately 1 week before symptoms develop. The incubation period varies from 2 to 9 weeks (mean duration, approximately 45 days). Until now, a few reports had described symptomatic hepatitis E acquired in Europe;5, 6 all patients with symptomatic hepatitis E in the United States were travelers returning from Mexico, Africa, or the Far East, in whom hepatitis E developed after their return home.7 In this issue of the Mayo Clinic Proceedings (pages 1133 to 1136), Kwo and associates describe a case of hepatitis E in a man who had not left the United States during the previous 10 years. Specific serologic tests for hepatitis E virus IgG (enzyme immunoassays and a fluorescent antibody blocking assay) and IgM8 (US strain-specific enzyme-linked immunosorbent assay with use of synthetic polypeptides deduced from the viral genome, as shown in Figure 1), developed at Abbott Laboratories (IgG and IgM) as well as at the Centers for Disease Control and Prevention (IgG), were used to prove that the patient indeed had acute hepatitis E. Researchers at Abbott Laboratories have prepared a report that describes most of the viral genome in this patient (Fig. I).8 Their results are interesting because this strain from the United States differs considerably from hepatitis E strains isolated in Mexico, Burma, Pakistan, or China. Furthermore, the sequence of the US strain is highly homologous (98% and 94% homology at the amino acid level to the second and third open reading frames, respectively) to a recently isolated hepatitis E strain from American swine.9 This finding suggests that, in the United States, hepatitis E is a zoonosis with the swine population as one of its hosts. This relationship would confirm earlier studies in Asia, where swine were also found to carry variants of the hepatitis E virus.10 Why are these two recent discoveries important for medicine in the United States? First, other sporadic, locally acquired cases of acute hepatitis may be caused by hepatitis E. Second, these back-to-back discoveries strongly suggest that a common natural host for hepatitis E is present in countries with more moderate climates. Because swine do not seem to experience any symptoms associated with infection and because symptoms in humans can be minor or absent, we now may also have an explanation for the 1 to 2% of positive hepatitis E serologic results in blood donors in the United States,11 Netherlands,12 and Italy,6 countries with large swine staples. Clearly, more research needs to be done to confirm this hypothesis. Third, in countries with more moderate climates, hepatitis E may often result in a subclinical infection. Is this variation in manifestation due to less virulent strains, and do sequence variations determine virulence? Fourth, swine may be used as an animal model for study of the disease as well as vaccine development.
Obesity is the abnormal condition that causes a person to put on excessive amounts of weight due to accumulation of fat in their body. This extreme weight causes a variety of other disorders and diseases as complications associated with it. https://goo.gl/GgSAoY
Graft-versus-host disease (GVHD) is a common complication after an allogeneic transplant, a transplant in which cells from a family member, unrelated donor or cord blood unit are used. In GVHD, the immune cells from the donated marrow or cord blood (the graft) attack the body of the transplant patient (the host).
Acute kidney injury is common entity in medical practice. The present definition is based on a serum creatinine rise of more 0.3 mg/dl in 48 hours or less, a 50% increase from the baseline over a period of 07 days or a urine output of less than 0.5 ml/kg/hour for more than 06 hours. The main causes of acute kidney injury may be classified into pre renal, intrinsic or post renal causes. Rapid diagnosis and prompt treatment is essential to prevent mortality or morbidity. This presentation discusses in detail the causes of all three mechanisms, pre-renal, post renal and intrinsic.
A stepwise approach to the causes and diagnosis of Anaemia in clinical practice. This presentation includes the all important concept of the Reticulocyte production index. Discussion of Hereditary and acquired causes of Anaemia has been included in detail.
To facilitate the delivery of fluids during labour, obstetric anaesthetists from Coventry designed a triple IV peripheral connector with a central high-flow anti-reflux valve. This connector, now rightly known as the Coventry valve, can be used for all theatre settings and is especially useful in obstetrics, ICU, HDU and orthopaedics. More details on www.mediplus.co.uk