Paternity Testing Procedure

To start a paternity test, simply call 1-800-613-5768 or use the online order form. Our client service team will take your information and arrange for convenient sample appointments; we can schedule separate appointments for different parties if required.

At the Collection Site
All test participants are asked to present government-issued identification (such as a Driver’s License) and to complete a Client Identification and Consent Form. The legal guardian must sign this form for test participants who are minors. The sample collector takes fingerprints and photographs of all test participants.

Buccal Swab Collection
Samples for a DNA test, such as a paternity test, are routinely collected using the painless and simple buccal swab—similar to a cotton-tipped swab, but made of the special material Dacron®. The swab is rubbed against the inside cheek of the test participant, and loose cheek cells adhere to the swab. Unlike regular cotton swabs, Dacron® provides a consistent surface for sample collection and DNA extraction.

DNA Test in the Laboratory
The sample collector sends the swabs to our laboratory in a sealed, tamper-evident package. When samples arrive in our laboratory, our staff checks to see if the package seal is intact. Each sample is recorded into our database. When all the samples for a paternity test case have arrived, we start the DNA test, which follows the following five steps:

• Samples from each person are divided in two for Dual Process™. From this point on, two independent laboratory teams take the samples through the DNA testing process.
• DNA is extracted from the buccal swabs and purified.
• The extracted DNA is added to a special chemical mix for the Polymerase Chain Reaction (PCR), a process that targets 16 specific locations in the DNA (called loci) and makes billions of copies of each location.
• The products of PCR are analyzed to create a DNA profile, a genetic equivalent of a fingerprint for each tested party.
• The child’s DNA profile is compared with the alleged father’s, and statistical analysis is performed to determine the probability of paternity. A 0% probability of paternity represents an exclusion (the alleged father is not the biological father) and at least a 99.99% probability represents an inclusion in a standard trio (the alleged father is the biological father).

Paternity Test Report
The paternity test results are ready within 3 working days (5 days for prenatal tests). We release the test results immediately, as long as the testing fees are fully paid. Results are sent via first-class mail; we also will send results through fax or courier upon request. Please call 1-800-613-5768 for instructions on requesting special delivery of results.

Signs and tests

Muscle wasting begins in the legs and pelvis, then progresses to the muscles of the shoulders and neck, followed by loss of arm muscles and respiratory muscles. Calf muscle enlargement (pseudohypertrophy) is quite obvious. Cardiomyopathy(DCM) is common, but the development of congestive heart failure or arrhythmias (irregular heartbeats) is only occasional.

    * A positive Gowers' sign reflects the more severe impairment of the lower extremities muscles. The child helps himself to get up with upper extremities: first by rising to stand on his arms and knees, and then "walking" his hands up his legs to stand upright.
    * Affected children usually tire more easily and have less overall strength than their peers.
    * Creatine kinase (CPK-MM) levels in the bloodstream are extremely high.
    * An electromyography (EMG) shows that weakness is caused by destruction of muscle tissue rather than by damage to nerves.
    * Genetic testing can reveal genetic errors in the Xp21 gene.
    * A muscle biopsy (immunohistochemistry or immunoblotting) or genetic test (blood test) confirms the absence of dystrophin, although improvements in genetic testing often make this unnecessary.

Mechanical ventilatory/Respiration Assistance

Modern "volume ventilators/respirators," which deliver an adjustable volume (amount) of air to the person with each breath, are valuable in the treatment of people with muscular dystrophy related respiratory problems. Ventilator treatment can begin in the mid to late teens when the respiratory muscles can begin to collapse. However there are people with the disease in their 20's who have no need for a ventilator.

If the vital capacity has dropped below 40 percent of normal, a volume ventilator/respirator may be used during sleeping hours, a time when the person is most likely to be under ventilating ("hypoventilating"). Hypoventilation during sleep is determined by a thorough history of sleep disorder with an oximetry study and a capillary blood gas (See Pulmonary Function Testing). The ventilator may require an endotracheal or tracheotomy tube through which air is directly delivered, however, for some people delivery through a face mask is sufficient.

If the vital capacity continues to decline to less than 30 percent of normal, a volume ventilator/respirator may also be needed during the day for more assistance. The person gradually will increase the amount of time using the ventilator/respirator during the day as needed. A tracheotomy tube may be used in the daytime and during sleep, however, delivery through a face mask may be sufficient. The machine can easily fit on a ventilator tray on the bottom or back of a power wheelchair with an external battery for portability.

Treatment for Duchenne muscular dystrophy

There is no known cure for Duchenne muscular dystrophy, although recent stem-cell research is showing promising vectors that may replace damaged muscle tissue. Treatment is generally aimed at controlling the onset of symptoms to maximize the quality of life, and include the following:

    * Corticosteroids such as prednisolone and deflazacort increase energy and strength and defer severity of some symptoms.
    * Randomised control trials have shown that beta2-agonists increase muscle strength but do not modify disease progression. Follow-up time for most RCTs on beta2-agonists is only around 12 months and hence results cannot be extrapolated beyond that time frame.[citation needed]
    * Mild, non-jarring physical activity such as swimming is encouraged. Inactivity (such as bed rest) can worsen the muscle disease.
    * Physical therapy is helpful to maintain muscle strength, flexibility, and function.
    * Orthopedic appliances (such as braces and wheelchairs) may improve mobility and the ability for self-care. Form-fitting removable leg braces that hold the ankle in place during sleep can defer the onset of contractures.
    * Appropriate respiratory support as the disease progresses is important

Symptoms of Duchenne muscular dystrophy

The main symptom of Duchenne muscular dystrophy, a progressive neuromuscular disorder, is muscle weakness associated with muscle wasting with the voluntary muscles[citation needed]  being first affected, especially affecting the muscles of the hips, pelvic area, thighs, shoulders, and calf muscles. Muscle weakness also occurs in the arms, neck, and other areas, but not as early as in the lower half of the body. Calves are often enlarged. Symptoms usually appear before age 6 and may appear as early as infancy. The other physical symptoms are:

    * Awkward manner of walking, stepping, or running. (patients tend to walk on their forefeet, because of an increased calf tonus. Also, toe walking is a compensatory adaptation to knee extensor weakness.)
    * Frequent falls
    * Fatigue
    * Difficulty with motor skills (running, hopping, jumping)
    * Increased Lumbar lordosis, leading to shortening of the hip-flexor muscles. This has an effect on overall posture and a manner of walking, stepping, or running.
    * Muscle contractures of achilles tendon and hamstrings impair functionality because the muscle fibers shorten and fibrosis occurs in connective tissue
    * Progressive difficulty walking
    * Muscle fibre deformities
    * Pseudohypertrophy(enlarging) of tongue and calf muscles. The enlarged muscle tissue is eventually replaced by fat and connective tissue, hence the term pseudohypertrophy.
    * Higher risk of behavior and learning difficulties, due to adjustment problems and muscular fatigue.
    * Eventual loss of ability to walk (usually by the age of 12)
    * Skeletal deformities (including scoliosis in some cases)

Duchenne muscular dystrophy

Duchenne muscular dystrophy (DMD) is a severe recessive X-linked form of muscular dystrophy  characterized by rapid progression of muscle degeneration, eventually leading to loss of ambulation and death. This affliction affects one in 3500 males, making it the most prevalent of muscular dystrophies. In general, only males are afflicted, though females can be carriers. Females may be afflicted if the father is afflicted and the mother is also a carrier/ affected. The disorder is caused by a mutation in the dystrophin gene, located in humans on the X chromosome (Xp21). The dystrophin gene codes for the protein dystrophin, an important structural component within muscle tissue. Dystrophin provides structural stability to the dystroglycan complex (DGC), located on the cell membrane.

Symptoms usually appear in male children before age 5 and may be visible in early infancy. Progressive proximal muscle weakness of the legs and pelvis associated with a loss of muscle mass is observed first. Eventually this weakness spreads to the arms, neck, and other areas. Early signs may include pseudohypertrophy (enlargement of calf and deltoid muscles), low endurance, and difficulties in standing unaided or inability to ascend staircases. As the condition progresses, muscle tissue experiences wasting and is eventually replaced by fat and fibrotic tissue (fibrosis). By age 10, braces may be required to aid in walking but most patients are wheelchair dependent by age 12. Later symptoms may include abnormal bone development that lead to skeletal deformities, including curvature of the spine. Due to progressive deterioration of muscle, loss of movement occurs eventually leading to paralysis. Intellectual impairment may or may not be present but if present, does not progressively worsen as the child ages. The average life expectancy for patients afflicted with DMD varies from late teens to early to mid 20s. There have been reports of a few DMD patients surviving to the age of 40, but this is extremely rare.[citation needed]