A Short Note On Glibenclamine

The hypothesis is that catalase activity will increase exponentially with higher concentrations of hydrogen peroxide until all catalase active sites are filled, in which case the

Catalase is an enzyme found in food such as potato and liver. It is used for removing Hydrogen Peroxide from the cells. Hydrogen Peroxide is the poisonous by-product of metabolism. Catalase speeds up the decomposition of Hydrogen Peroxide into water

The purpose of this lab is to investigate the composition of a compound suspected to be Panacetin, a type of pain-killer. Panacetin is typically made up of sucrose, aspirin, and acetaminophen, but the third component in this experiment is unknown. The unknown component is suspected to be a chemical relative of acetaminophen, either acetanilide or phenacetin. Using techniques such as extraction, evaporation, and filtration, the three components will be isolated based on their solubilities and acid-base properties. Then, the percent composition of Panacetin can be deduced based on the masses of the three dried components. The

The purpose of this investigation is to discover the effect of pH on the activity of catalase, an enzyme which plays the integral role of converting hydrogen peroxide into water and oxygen, and discover which pH level it will work at the most efficient rate (the optimum). The original hypothesis states that that the optimum would be at a pH is 7, due to the liver, where catalase usually resides, being neutral. The experiment consists of introducing the catalase to hydrogen peroxide, after exposure to certain solutions; hydrogen peroxide, water and hydrochloric acids, all containing the adjusted pH, and measuring the height of froth formed, an observable representation of the activity of the enzyme. The final data indicated that

Running the chloroform extracts and diluted sample together with two positive controls and a negative control on a single chromatographic plate simultaneously, the retention factor(Rf) of five different samples were determined. The RF value of the chloroform extract(0.75) tallied with that of the codeine positive control and that of diluted sample(1.00) with the paracetamol positive control.

Acting in accordance with National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), diabetic neuropathies are family of nerve syndromes affected by diabetes (2009). People with diabetes can be asymptomatic overtime and some can have notable signs with radicular symptoms in the upper and lower extremities (NIDDK, 2009), Moreover, can affect even the digestive, cardiac, and reproductive system in serious conditions (NIDDK, 2009). In fact, based on academic literatures, about two thirds of patients with diabetes have medical or subclinical pathology of nerve (Bansal, Kalita, & Mistra, 2006). The occurrence of neuropathy amplified from approximately 7 percent to 50 percent on admittance at 25 years in consequence (Bansal, Kalita, & Mistra, 2006).

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Globally, The number of patients with diabetes is increasing rapidly. By the year 2035, the number of people with diabetes worldwide is expected to rise to 592 million (IDF ATLAS 20131). Diabetic peripheral neuropathy (DPN) is a common microvascular complication of diabetes and a leading cause to amputations in hospitals (Boulton 20052). The prevalence of DPN is estimated to be 50-60% (Sandireddy R 20143). The pain associated with DPN can affect the patient quality of life (QOL). It affects their sleep, lifestyle, work and even can cause or be associated with depression (Jensen MP 20074). It is not well understood whether the mechanism behind peripheral neuropathy with diabetes is hyperglycemia or other insulting pathophysiological mechanism like proinflamatory immune mediators (Herder C 20135, Goh S-Y 20086). One of the possible mechanisms is the demyelination of the small C fiber, this is the leading cause behind the pain sensation with

One of the most common long-term complications of diabetes mellitus is painful neuropathy. Diabetic neuropathy is estimated to affect about 60-70% of all diabetes patients and can lead to foot ulcers, amputations, and decreased quality of life. The most common form is chronic peripheral neuropathy which results in pain and numbness in the extremities, usually described as a burning, tingling, or steady aching pain.1 Patients may also feel increased sensitivity to pain or experience paresthesia, a sensation of tingling, tickling, or prickling of the skin.1 According to current guidelines, intensive glycemic control is very important for the prevention and reduction of peripheral neuropathy and other microvascular complications.1,2 Medications used to help relieve nerve pain include duloxetine and pregabalin (Lyrica®), which are both approved by the U.S. Food and Drug Administration for use in diabetic neuropathy. Other drug classes commonly used are antidepressants, anticonvulsants, and opioids.3 Although there are many medications used for this condition, pain relief is often insufficient for patients. Treatment is difficult due to the complicated pathophysiology of pain transmission and the wide range of mechanisms of action of drugs used to treat pain. Therefore, there is a continued need for additional medication options for this chronic painful condition. Lacosamide is an anticonvulsant approved for use as monotherapy or adjunctive therapy for partial-onset seizures.

Diabetic peripheral neuropathy (DPN) is the most common type of diabetic neuropathy (NIH, 2009). Chronically high levels of blood sugar lead to nerve damage not only in the extremities, but also in other parts of the bodies. This damage occurs in an approximate 60% to 70% of all diabetic patients, eventually, developing into peripheral neuropathy (WebMD,2013). These damaged nerves have trouble effectively transfer messages between the brain and other parts of the body, which means DNP patients are prone to unaware the sores or injuries in the feet until infected. Also, this form of neuropathy patients has a high risk of pain and autonomic dysfunction. DPN is a progressive, poorly reversible or irreversible complication and no approved drugs could be used to reverse or halt the progression of it. It is the most frequent reason for seeking medical concerns and

Nerve damage from diabetes is called diabetic neuropathy. About half of all people with diabetes have some form of nerve damage. It is more common in those who have had the disease for a number of years and can lead to many kinds of problems.If you keep your blood glucose levels on target, you may help prevent or delay nerve damage. If you already have nerve damage, this will help prevent or delay further damage (ADA,2016). I've encountered patients that describe the feeling as pins and needles, and that their feet are constantly cold. There isn't medication to cure the nerve damage that causes neuropathy, however certain mediction can be precribed by your physician that will help with the symptoms. Increased blood glucose levels damages blood

Adult mice between 8–24 weeks of age were used and handled in accordance with the IACUC

Diabetic peripheral neuropathy is among the chronic microvascular complications of diabetes mellitus due to hyperglycemia. Prevalence of diabetic neuropathy is high, affecting more than 60% of diabetics (Boulton et al., 2005). The clinical manifestation of diabetic neuropathy include numbness, tingling sensation in toes, feet, legs, arms, hands and fingers (Kumar et al.). It leads to significant morbidity, impact on quality of life of patients (Zychowska et al.) and increases the risk of infections leading to the foot ulcers and non traumatic amputations (Bansal et al.).

Hyperglycemia is known to adversely affect peripheral nerve structure and function in younger (3–6 months) but not in older rats. Physical and functional damage to peripheral nerves associated with diabetes is related to increased activity of the polyol pathway . The polyol pathway is a minor pathway of glucose metabolism that increases the intracellular content of the polyol sorbitol in response to increased extracellular glucose concentrations.

Tail flick test is an acute model of pain. In this study it was used to assess the anti-nociceptive effect of the drugs by measuring the latency of response (18). In this method, animal tail is exposed to a powerful light beam and the response latency period for flicking the tail off the beam is recorded (19). We apply radiant heat to the tail at 5-8 cm from the tip by using a tail flick apparatus. Tail flick latency time was estimated as the time from the onset of the heat exposure to the withdrawal of the tail. They adjusted the intensity of radiant heat to yield the baseline latencies of 2-4 sec. In order to avoid tissue damages the heat stimulus was discontinued after 7 sec (Cut off point =7 sec). In this study, tail flicking done 30,