Hepatitis C is an infectious disease caused by the hepatitis C virus that affects the liver. During the initial infection people have mild or no symptoms. A fever, dark urine, abdominal pain, yellow tinged skin occurs; the virus persists in the liver in about 75% to 85% of those infected. Early on chronic infection has no symptoms. Over many years however, it leads to liver disease and cirrhosis. In some cases, those with cirrhosis will develop serious complications such as liver failure, liver cancer, or dilated blood vessels in the esophagus and stomach. HCV is spread by blood-to-blood contact associated with intravenous drug use, poorly sterilized medical equipment, needlestick injuries in healthcare, transfusions. Using blood screening, the risk from a transfusion is less than one per two million, it may be spread from an infected mother to her baby during birth. It is not spread by superficial contact, it is one of five known hepatitis viruses: A, B, C, D, E. Diagnosis is by blood testing to look for either antibodies to the virus or its RNA.

Testing is recommended in all people. There is no vaccine against hepatitis C. Prevention includes harm reduction efforts among people who use intravenous drugs and testing donated blood. Chronic infection can be cured about 95% of the time with antiviral medications such as sofosbuvir or simeprevir. Peginterferon and ribavirin were earlier generation treatments that had a cure rate of less than 50% and greater side effects. Getting access to the newer treatments however can be expensive; those who develop cirrhosis or liver cancer may require a liver transplant. Hepatitis C is the leading reason for liver transplantation, though the virus recurs after transplantation. An estimated 143 million people worldwide are infected with hepatitis C as of 2015. In 2013, about eleven million new cases occurred, it occurs most in Africa and Central and East Asia. About 167,000 deaths due to liver cancer and 326,000 deaths due to cirrhosis occurred in 2015 due to hepatitis C; the existence of hepatitis C – identifiable only as a type of non-A non-B hepatitis – was suggested in the 1970s and proven in 1989.

Hepatitis C infects only chimpanzees. Acute symptoms develop in some 20-30% of those infected; when this occurs, it is 4–12 weeks following infection. Symptoms are mild and vague, may include fatigue and vomiting, muscle or joint pains, abdominal pain, decreased appetite and weight loss, dark urine, clay-coloured stools. There is no evidence that acute hepatitis C can alone cause acute liver failure, though liver injury and elevated liver enzymes may occur. Symptoms and laboratory findings suggestive of liver disease should prompt further tests and can thus help establish a diagnosis of hepatitis C infection early on. Following the acute phase, the infection may resolve spontaneously in 10–50% of affected people. About 80% of those exposed to the virus develop a chronic infection; this is defined as the presence of detectable viral replication for at least six months. Most experience minimal or no symptoms during the initial few decades of the infection. Chronic hepatitis C can be associated with fatigue and mild cognitive problems.

Chronic infection after several years may cause cirrhosis or liver cancer. The liver enzymes are normal in 7–53%. Late relapses after apparent cure have been reported, but these can be difficult to distinguish from reinfection. Fatty changes to the liver occur in about half of those infected and are present before cirrhosis develops; this change affects less than a third of the liver. Worldwide hepatitis C is the cause of 25 % of hepatocellular carcinoma. About 10–30% of those infected develop cirrhosis over 30 years. Cirrhosis is more common in those infected with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male gender. In those with hepatitis C, excess alcohol increases the risk of developing cirrhosis 100-fold; those who develop cirrhosis have a 20-fold greater risk of hepatocellular carcinoma. This transformation occurs at a rate of 1–3% per year. Being infected with hepatitis B in addition to hepatitis C increases this risk further. Liver cirrhosis may lead to portal hypertension, easy bruising or bleeding, jaundice, a syndrome of cognitive impairment known as hepatic encephalopathy.

Ascites occurs at some stage in more than half of those. The most common problem due to hepatitis C but not involving the liver is mixed cryoglobulinemia — an inflammation of small and medium-sized blood vessels. Hepatitis C is associated with autoimmune disorders such as Sjögren's syndrome, lichen planus, a low platelet count, porphyria cutanea tarda, necrolytic acral erythema, insulin resistance, diabetes mellitus, diabetic nephropathy, autoimmune thyroiditis, B-cell lymphoproliferative disorders. 20–30% of people infected have rheumatoid factor — a type of antibody. Possible associations include Hyde's prurigo nodularis and membranoproliferative glomerulonephritis. Cardiomyopathy with associated abnormal heart rhythms has been reported. A variety of central nervous system disorders has been reported. Chronic infection seems to be associated with an increased risk of pancreatic cancer. People may experience other issues in the mouth such as dryness, salivary duct stones, crusted lesions around the mout

Waterloo was launched in 1815 at Plymouth. She made two voyages to India. Heavy seas in October 1820 so damaged her. Waterloo first appeared in Lloyd's Register in 1815 with Rutledge and master, trade Plymouth–London. In 1813 the EIC had lost its monopoly on the trade between Britain. British ships were free to sail to India or the Indian Ocean under a license from the EIC. Captain J. Burney sailed for Fort William, India in April 1817. On 1 April she was at Portsmouth. On 23 August she arrived at Madras. On 24 February 1818 she returned to Deal from Madras. LR for 1818 showed Waterloo with J. Burney, master, P. Grant and trade London–Île de France. Captain J. Hepburne sailed from London for Fort William on 24 May 1818. A report had her sailing to Madras. On 18 September 1818 Waterloo, master, was reported to have arrived at the Sunda Strait from London. On 30 September 1819 Waterloo arrived at Liverpool from Madras; the Register of Shipping for 1820 showed Waterloo with Hepburn, Grant & Co. owners, trade London–India.

LR for 1820, showed her master changing from J. Burney to W. Martin, her trade from London–Île de France to Liverpool–New Orleans. LR for 1822, with stale data, showed Waterloo with W. Martin, Duff & Co. owners, trade Liverpool–New Brunswick. On 24 October 1820 Waterloo, master, was on a voyage from Saint John, New Brunswick, to Liverpool when a heavy sea struck her at 46°26′N 25°0′E and carried away her lower masts and swept her deck. On the 30th three people were swept overboard and she lost her rudder; as she was now unmanageable her crew took to her boats. Merchant rescued the survivors. Merchant, an American ship from New York, rescued the survivors. One source attributes to this Waterloo the fate of Waterloo. Citations References Hackman, Rowan. Ships of the East India Company. Gravesend, Kent: World Ship Society. ISBN 0-905617-96-7

This article provides details on the middle schools within the Prince George's County Public Schools system, in the U. S. State of Maryland. Middle schools operate as either 6th -- 8th grade 7th -- 8th grade middle schools; some middle schools are part of combined PreK-8th grade elementary/middle schools, are referred to as "Academies". Grades 7–9 junior high schools were phased out in the mid-1980s. Recent efforts have been made to convert most middle schools to the more popular grades 6–8 model. Issues in the past such as over-enrollment, lack of classroom space, funding, had made it hard to convert all middle schools to a grades 6–8 configuration, but with increased funding and the addition of new middle schools, the transition is being made; as of SY2008–2009, more than half of the PGCPS middle schools have gained the sixth grade. Most middle schools in Prince George's County operate with a "comprehensive" model as their base. Most students are assigned to a middle school based on an "attendance area".

Most magnet programs are run as a "school-within-a-school" model, where the magnet serves as an alternative program — in addition to the main comprehensive program — and students from outside the regular attendance area of the middle school are enrolled and accepted into the magnet, either through continuity or more through a "magnet lottery", where students apply for a magnet program and are granted acceptance through a random drawing. All middle schools have a whole-school "signature program" that includes a specialized program of instruction, the foundation of the school's comprehensive program. All middle schools in the PGCPS operate on a staggered school day schedule, where some middle schools start as early as 7:45 am and the end as early as 2:25 pm, other middle schools start as late as 9:30 am and end as late as 4:10 pm. All middle schools operate on a modified block scheduling system, where some classes meet for as long as 70 minutes, daily. In a cooperative effort of the county government, Board of Education, the Maryland-National Capital Park & Planning Commission, some M-NCPPC community centers are physically connected to middle schools throughout the district.

The unique community park/school centers features shared use areas which include a gymnasium, multi-purpose room, exercise/fitness room, dance room and crafts room, computer lab, storage areas, patio area, restrooms. There are unlighted fields located on-site at select centers; the Accokeek Academy is a Gifted Center magnet school, located in Accokeek. The Accokeek Academy was instituted in the fall of 2009 as part of the PGCPS school consolidation effort. Under the initiative, Eugene Burroughs Middle School and neighboring Henry G. Ferguson Elementary School were combined to create The Accokeek Academy; the school's name was decided after input from the community. At the middle school-level, the principal is Judy Adams; the school hours are 9:30 am – 4:10 pm. There are 700 students enrolled in grades 6–8; the school has a uniform policy in place. The Talented and Gifted Magnet Program at the Accokeek Academy is designed to provide accelerated learning for gifted students; the program functions as a "school-within-a-school," where the magnet serves as a secondary program to the main comprehensive program.

Admission into the TAG magnet program is through specialized TAG admissions testing only. In 2009, 73.6% and 52% of all students in Grades 6–8 tested proficient in reading and mathematics based on scores from the state-administered MSAs. 32 % of all students were eligible for the government-funded reduced lunch program. Half of all students attend high school at Friendly High School, while the other half attend Gwynn Park High School. Beltsville Academy is a pre-kindergarten through 8th grade academy, located in Beltsville. Beltsville Academy operated as Beltsville Elementary School and prior to that, as Beltsville Academic Center, until the 2008–09 school year, when it was converted to a pre-kindergarten through 8th grade school; the middle school comprises grades six through eight. The principal is Rashida Edwards; the school hours are 8:30. This school does not have a uniform policy. Beltsville Academy is a feeder school to High Point High School. Buck Lodge Middle School is a Title I comprehensive school located in Adelphi.

The principal is James Richardson. The school hours are 8:30. 643 students are enrolled. There is a mandatory uniform policy in effect at this school; as of 2009, 69.1% and 56.2% of all students were proficient in reading and mathematics as determined by the statewide MSA assessments. Buck Lodge Middle School only serves the communities of Adelphi and Langley Park. Langley Park McCormick Elementary School, Mary Harris Mother Jones Elementary School, Cool Spring Elementary School, Adelphi Elementary School, Cherokee Lane Elementary School are all feeder schools into Buck Lodge Middle School. Buck Lodge Middle School feeds into High Point High School. Charles Carroll Middle School is a Title I comprehensive middle school, located in New Carrollton; the school is named after Charles Carroll of Carrollton, a lawyer, delegate to the Continental Congress, United States Senator for Maryland. The principal is Jr.. There is a mandatory uniform policy in e