CAYENNE FOR MUSCULAR PAIN AND TENSION

INTRODUCTION: Cayenne (Capsicum annum), also known as chili pepper, paprika, or red pepper, has been used as a remedy for minor muscle pain or tension. Capsaicin, the active ingredient in cayenne, diminishes the chemical messengers that travel through the sensory nerves, thereby decreasing the sensation of pain. A review of the existing literature concluded that capsaicin is effective in reducing neuropathic pain when used topically as a repeated application at low doses (0.075%), or as a single application of a high dose. Capsaicin cream (0.025% to 0.075%) is available over the counter and may be applied directly to the affected area up to four times a day. The highest dose (8%) is available as a patch by prescription and its use must be carefully monitored by a health care provider. The topical creams are well tolerated, with reddening of the skin and local stinging being the most common side effects. It should be kept away from the eyes and mucous membranes to avoid burning, and the hands must be washed thoroughly after use.

RELATED;

1.  BACK PAIN  

2.  CARNITINE FOR HEART DISEASE

3.  TRADITIONAL AND COMPLIMENTARY MEDICATIONS

REFERENCES

TRANSCRIPTION AND TRANSLATION

 

INTRODUCTION: Messanger RNA (mRNA); The gene present in DNA is transcribed into mRNA. This constitutes about 2-5% of total RNA in the cell. They are generally degraded quickly. Ribosomal RNA (rRNA); This constitutes about 80% of all RNA in the cell. 28S, 18S and 5S are the major varieties. They are involved in the protein biosynthesis. Transfer RNA (tRNA). There are about 60 different species present. They constitute about 15% of the total RNA in the cell. They are very stable. Small RNA. They constitute about 1-2% of total RNA in the cell. There are about 30 different varieties. They are very stable. Small Nuclear RNAs (SnRNAs) are a subgroup of small RNA. Some important species of SnRNAs are U1 (165 nucleotides), U2 (188 nucleotides), U3 (216), U4 (139), U5 (118), U6 (106). They are involved in mRNA splicing.

CENTRAL DOGMA OF MOLECULAR BIOLOGY: Here, the information available in the DNA is passed to messenger RNA, which is then used for synthesis of a particular protein.

REPLICATION, TRANSCRIPTION AND TRANSLATION: DNA replication is like printing a copy of all the pages of a book. The replication process occurs only at the time of cell division. But transcription is taking place all the time. Only certain areas of the DNA are copied that is to say, selected regions on the sense strand. This is like taking a copy of particular page of the book. So, the genetic information of DNA is transcribed or copied to the messenger RNA (mRNA). During transcription, the message from the DNA is copied in the language of nucleotides (4 letter language).

The mRNA then reaches the cytoplasm where it is translated into functional proteins. During translation, the nucleotide sequence is translated to the language of amino acid sequence or 20 letter language.

TEMPLATE AND CODING STRANDS: The template strand is transcribed to give rise to mRNA. The template strand has the complementary sequence of mRNA. Then the opposite strand has the same sequence as the mRNA. The DNA strand having the same sequence of mRNA is called coding strand. As it is complementary to the template strand, it is also called antitemplate strand or nontemplate strand.

Messenger RNA or mRNA: It acts as a messenger of the information in the gene in DNA to the protein synthesizing machinery in cytoplasm. It carries the message to be translated to a protein. The template strand of DNA is transcribed into a single stranded mRNA. This is accomplished by the enzyme, DNA dependent RNA polymerase. The mRNA is a complementary copy of the template strand of the DNA. However, thymine is not present in RNA and instead Uracil will be incorporated.

RELATED;

1.  THE HUMAN DNA

2.  STRUCTURE OF RNA

3.  BIOCHEMISTRY OF NUCLEOTIDES

4.  BIOCHEMISTRY

REFERENCES

HOW TO CREATE A WINDOWS 10 BOOTABLE USB DISC

HOW TO CREATE A BOOTABLE USB DISC:  Installing windows now days does not require sophisticated steps like it used to be during times of using CDs and DVDs.  And although many people in different parts of the World may still prefer using CDs and DVDs, the bootable flash method proves more efficient and reliable.  You can easily install a Windows package from your flash drive onto your new or old computer with less hassle.  But before you do that, you need to have the Windows software pack built on the flash drive, and then it will be called as "bootable USB drive".  In this discussion, I am going to show you how you can make yourself a bootable USB disc for installation of Windows 10, 8 or even 7.

Requirements:

1.  Windows disc image:  The windows 10 image file is the one that will be built onto the USB flash drive to make it bootable.  If you have the Windows 10 Installation files on a DVD, on the PC or any media and it is is not in ISO format, you can convert it to ISO format using some of the tools mentioned in the link below.  How to make Windows 10 ISO file for installation media creation

2.  A removable USB drive 6GB or larger:  Although for some other windows the ISO file may be a little less, the Windows 11 ISO file is a little more than 5 GB and therefore you will need a flash drive 6GB or more.

3.  PC running windows 10 or higher:  To create the bootable USB drive, you will need another PC running windows.

4.  PC onto which window will be installed

5.  Tool for marking the bootable USB drive:  You will also need a tool to do the work for you and although there are dozens of tools for that purpose, I recommend Rufus tool for simplicity

Steps:

1.  Extract and run the tool, rufus in that case

2.  Format your USB flash disk which is more than 6GB for the latest operating systems

3.  In the tool, make sure you allocate and select the source of the Windows ISO file

4.  As long as the Downloaded ISO file is not modified, leave the rest of the settings as they are and select next.

5.  The after the tool has finished, you can continue booting your PC from the flash drive to install windows.

RUFUS TOOL

Download setup

RELATED;

1.  FULL USE OF WINDOWS INBUILT TOOLS

2.  RUFUS TOOL

3.  HOW TO ENTER THE BIOS MENU ON ASUS

FLOROQUINOLONES

INTRODUCTION: Although the first drug in this class, nalidixic acid, was approved by the FDA in 1962, it had a narrow spectrum of activity, and its use was restricted to UTIs. Nalidixic acid is still used for the pharmacotherapy of UTI, although it is not a preferred drug for this infection. Since then, four generations of fluoroquinolones have become available, differing in their antibacterial spectrums. All fluoroquinolones have activity against gram-negative pathogens; the newer ones are significantly more effective against gram-positive microbes, such as staphylococci, streptococci, and enterococci. Enterobacteriaceae

SPECTRUM OF ACTIVITY: The fluoroquinolones are bacteriocidal and affect DNA synthesis by inhibiting two bacterial enzymes: DNA gyrase and topoisomerase IV.

CLINICAL APPLICATIONS: Clinical applications of fluoroquinolones include infections of the respiratory, GI, and genitourinary tracts, and some skin and soft-tissue infections. Their effectiveness against gram-negative organisms makes them preferred drugs for the treatment of uncomplicated UTIs. A newer drug in this class, moxifloxacin (Avelox), is effective against anaerobes, a group of bacteria that are often difficult to treat. The most widely used fluoroquinolone, ciprofloxacin (Cipro), is a drug of choice for the postexposure prophylaxis of Bacillus anthracis, the organism responsible for causing anthrax. Bacillus spp

Ciprofloxacin is also indicated for postexposure prophylaxis to other potential biologic warfare pathogens such as Yersinia pestis (plague), Francisella tularensis (tularemia), and Brucella melitensis (brucellosis). Two drugs in this class, gatifloxacin and besifloxacin, are available only as drops to treat infections of the external eye.

PHARMACOKINETICS: A major advantage of the fluoroquinolones is that most are well absorbed orally and may be administered either once or twice a day. Although they may be taken with food, they should not be taken concurrently with multivitamins or mineral supplements because calcium, magnesium, iron, or zinc ions can reduce the absorption of some fluoroquinolones by as much as 90%. Fluoroquinolones are well tolerated by most patients, with nausea, vomiting, and diarrhea being the most common adverse effects. The most serious adverse effects are dysrhythmias (moxifloxacin) and potential hepatotoxicity.

CNS effects such as dizziness, headache, and sleep disturbances affect 1% to 8% of patients. Most recently, fluoroquinolones have been associated with cartilage toxicity with an increased risk of tendonitis and tendon rupture, particularly of the Achilles tendon. The risk of tendon rupture is increased in patients over age 60 and those receiving concurrent corticosteroids. Because animal studies have suggested that fluoroquinolones affect cartilage development, these drugs are not approved for children under age 18. Use in pregnancy or in lactating patients should be avoided.

RELATED;

1.  DRUG USE AND PREGNANCY  

2.  SALFONAMIDES

3.  PHARMACOLOGY AND THERAPEUTICS

REFERENCES

MAJOR HISTOCOMPATIBILITY COMPLEX (MHC)

 

INTRODUCTION: By virtue of genetic make-up, every individual has unique antigens on the cell surfaces. Some of these are called as histocompatibility (histo: tissue) antigens. These are responsible for determining whether one tissue is compatible with another. In human beings these antigens are called as human leukocyte antigens (HLA). Expression of histocompatibility antigens is controlled by genes or groups of genes (loci) located close together (linked) on the same chromosomal strand. This segment of chromosome is called major histocompatibility complex, or MHC.

LINK IN HUMAN GENES: In humans MHC is called as HLA complex and is located on chromosome 6. This is large, complex genetic region that controls not only the exchange of tissues but also diverse cellular interactions of human cells, production of certain serum proteins, and production of few cytokines and enzymes.  Certain HLA antigens are also related to increased susceptibility to specific diseases. With the help of standard antisera, HLA types of an individual can be ascertained. An important medical application of HLA typing is transplantation where the donor and the recipient must be matched. Every individual will have a unique pattern of HLA type. The existence of HLA antigens in humans denotes the presence of a system which recognises these as self and does not reject these.

RELATED;

1.  IMMUNITY   

2.  AUTOIMMUNITY 

3.  AUTOIMMUNE DISEASE

4.  MEDICAL MICROBIOLOGY 

REFERENCES

STREPTOMYCIN

 

INTRODUCTION:  Streptomycin was isolated from a strain of Streptomyces griseus. The antimicrobial activity of streptomycin is typical of that of other aminoglycosides, as are the mechanisms of resistance.  Resistance has emerged in most species, severely limiting the current usefulness of streptomycin. Ribosomal resistance to streptomycin develops readily, limiting its role as a single agent.

CLINICAL USES:  

A. Mycobacterial Infections; Streptomycin is mainly used as a second-line agent for treatment of tuberculosis. The dosage is 0.5–1 g/d (7.5–15 mg/kg/d for children), which is given intramuscularly or intravenously. It should be used only in combination with other agents to prevent emergence of resistance.

B. Non-tuberculous Infections:  In plague, tularemia, and sometimes brucellosis, streptomycin, 1 g/d (15 mg/kg/d for children), is given intramuscularly in combination with an oral tetracycline. Penicillin plus streptomycin is effective for enterococcal endocarditis and 2-week therapy of viridans streptococcal endocarditis. Gentamicin has largely replaced streptomycin for these indications.  Streptomycin remains a useful agent for treating enterococcal infections, however, because approximately 15% of enterococcal isolates that are resistant to gentamicin (and therefore resistant to netilmicin, tobramycin, and amikacin) will be susceptible to streptomycin.

ADVERSE REACTIONS:  Fever, skin rashes, and other allergic manifestations may result from hypersensitivity to streptomycin. This occurs most frequently with prolonged contact with the drug either in patients who receive a prolonged course of treatment (eg, for tuberculosis) or in medical personnel who handle the drug. Desensitization is occasionally successful. Pain at the injection site is common but usually not severe. The most serious toxic effect with streptomycin is disturbance of vestibular function; vertigo and loss of balance. The frequency and severity of this disturbance are in proportion to the age of the patient, the blood levels of the drug, and the duration of administration. Streptomycin given during pregnancy can cause deafness in the newborn and, therefore, is relatively contraindicated.

 

RELATED;

1.  TUBERCULOSIS

2. ANTITUBERCULAR DRUGS

3. BRUCELLOSIS

4. GENTAMYCIN

5. DRUG USE IN RELATION TO PREGNANCY

6. ANTIMICROBIAL DRUG RESISTANCE

REFERENCES

ALDOSTERONE

INTRODUCTION: Aldosterone is the most abundant of the mineralocorticoids, and we will use it as a representative of this group of hormones. The target organs of aldosterone are the kidneys, but there are important secondary effects as well.

ROLE OF THE HORMONE IN THE BODY: Aldosterone increases the reabsorption of sodium and the excretion of potassium by the kidney tubules. Sodium ions (Na) are returned to the blood, and potassium ions (K) are excreted in urine. As Na ions are reabsorbed, hydrogen ions (H) may be excreted in exchange. This is one mechanism to prevent the accumulation of excess H ions, which would cause acidosis of body fluids. Also, as Na ions are reabsorbed, negative ions such as chloride (Cl) and bicarbonate (HCO3–) follow the Na ions back to the blood, and water follows by osmosis. This indirect effect of aldosterone, the reabsorption of water by the kidneys, is very important to maintain normal blood volume and blood pressure.

SUMMERY OF ROLES: In summary, then, aldosterone maintains normal blood levels of sodium and potassium, and contributes to the maintenance of normal blood pH, blood volume, and blood pressure.

STIMULATION OF SECRETION: A number of factors stimulate the secretion of aldosterone. These are a deficiency of sodium, loss of blood or dehydration that lowers blood pressure, or an elevated blood level of potassium. Low blood pressure or blood volume activates the renin-angiotensin mechanism of the kidneys.

Angiotensin II causes vasoconstriction and stimulates the secretion of aldosterone by the adrenal cortex. Aldosterone then increases sodium and water retention by the kidneys to help restore blood volume and blood pressure to normal.

RELATED;

1.  CATALASE  

2.  GLUCAGON  

3.  CONTROL OF BLOOD PRESSURE

4.  BIOCHEMISTRY

REFERENCES

BACTERIAL CELL WALL

INTRODUCTION: The tasks of the complex bacterial cell wall are to protect the protoplasts from external environment, to withstand and maintain the osmotic pressure gradient between the cell interior and the extracellular environment keeping internal pressures as high as 500–2000kPa, to give the cell its outer form and to facilitate communication with its surroundings.

MUREIN, ALSO KNOWN AS PEPTIDOGLYCAN: The most important structural element of the wall is murein, a netlike polymer material surrounding the entire cell. It is made up of polysaccharide chains crosslinked by peptides.

THE CELL WALL OF GRAM-POSITIVE BACTERIA: The murein sacculus may consist of as many as 40 layers or 15–80 nm thick and account for as much as 30% of the dry mass of the cell wall. The membrane lipoteichoic acids are anchored in the cytoplasmic membrane, whereas the cell wall teichoic acids are covalently coupled to the murein. The physiological role of the teichoic acids is not known in detail; possibly they regulate the activity of the autolysins that steer growth and transverse fission processes in the cell.

THE CELL WALL OF GRAM-NEGATIVE BACTERIA: Here, the murein is only about 2nm thick and contributes up to 10% of the dry cell wall mass. The outer membrane is the salient structural element. It contains numerous proteins (50% by mass) as well as the medically critical lipopolysaccharide. Outer membrane-associated proteins (Omps) constitute specific structures that enable bacteria to attach to host cell receptors. A number of Omps are transport proteins. This molecular complex, also known as endotoxin, is comprised of the lipoid A, the core polysaccharide, and the O-specific polysaccharide chain.

RELATED;

1.  BACTERIOLOGY  

2.  WATCH A VIDEO DEMONSTRATION OF THE BACTERIAL CELL MEMBRANES

3.  GRAM NEGATIVE BACTERIA

PYRUVATE

 

INTRODUCTION:  Pyruvic acid (CH₃COCOOH) is the simplest of the α-keto acids, with a carboxylic acid and a ketone functional group. Pyruvate, the conjugate base, CH₃COCOO−, is a key intermediate in several metabolic pathways. In glycolysis, one molecule of glucose breaks down into two molecules of pyruvate, which are then used to provide further energy, in one of two ways.

SOURCES OF PYRUVATE: Pyruvate is converted into acetyl-coenzyme A, which is the main input for a series of reactions known as the citric acid cycle. Pyruvate is also converted to oxaloacetate by an anaplerotic reaction, which replenishes citric acid cycle intermediates. Also, the oxaloacetate is used for gluconeogenesis. If insufficient oxygen is available, the acid is broken down anaerobically, creating lactate in animals and ethanol in plants and microorganisms.

DESTINATION OF PYRUVATE:  Pyruvate from glycolysis is converted by fermentation to lactate using the enzyme lactate dehydrogenase and the coenzyme NADH in lactate fermentation, or to acetaldehyde and then to ethanol in alcoholic fermentation. Pyruvate is a key intersection in the network of metabolic pathways. Pyruvate can be converted into carbohydrates via gluconeogenesis, to fatty acids or energy through acetyl-CoA, to the amino acid alanine, and to ethanol. Therefore, it unites several key metabolic processes. Pyruvic acid supplies energy to cells through the citric acid cycle (also known as the Krebs or TCA cycle) when oxygen is present (aerobic respiration), and alternatively ferments to produce lactate (in mammals) when oxygen is lacking (fermentation). 

RELATED;

1.  lacticacid/lactate  

2.  Citric acid cycle

3.  Biochemistry

REFERECES

METABOLIC PROFILE OF ORGANS

 

INTRODUCTION: The metabolic pattern or metabolic profile of different organs is different depending on its function. Moreover, the organs are able to adapt to metabolic alterations in fed state and starvation. Calories are stored in the body as fat and glycogen. The approximate percentage of storage form of energy otherwise known as total fuel reserve present in a normal human body is, fat 85%, glycogen 1%, and proteins 14%. 

[glycogen] [proteins] [fats]

Fat stores are mobilized actively only on prolonged fasting, even though adipose tissue fat is undergoing turnover on a daily basis. Caloric homeostasis is maintained regardless of whether a person is well fed, fasting, or in a state of starvation. Similarly metabolic profile of various organs and tissues change to adapt to physiological and pathological states, so that caloric homeostasis is maintained unless extreme conditions set in. The reciprocal regulation of glycolysis and gluconeogenesis is the major deciding factor in the flux of metabolic intermediates through these pathways. 

[glycolysis]

Brain: First, although brain represents only 2% of adult body weight, it needs 10–20% cardiac output. About 750 ml of blood circulates through the brain per minute. Neurons can survive only a few minutes without blood supply. Occlusion of blood supply to brain causes unconsciousness within 10 seconds. Secondly, there is no stored fuel in the brain. Glucose, the preferred fuel for the brain, should be in continuous supply. Glucose can freely enter the brain cells. 

[the blood brain barrier] 

To add on, the total consumption of glucose by brain is about 120 g/day (480 kcal). Thus, about 60% of the total carbohydrate intake by the body is metabolized by the brain. Moreover, about 25% of the oxygen consumed by the adult body is due to glucose oxidation in brain. In children, this may be as high as 50% however.

Brain under conditions of anoxia: In anoxia the rate of lactate production by glycolysis rises to 5 or 8 times within one minute. 

[lactate]

Brain and acetoacetate: The brain is unable to utilize fatty acids as a source of fuel since the fatty acids complexed to albumin are unable to traverse the blood brain barrier. [blood brain barrier] 

But, brain can effectively utilize acetoacetate. This is again a survival technique in diabetic and starvation ketosis.

Brain and starvation: During starvation, a significant part (60-70%) of the energy requirement of the brain is then met by ketone bodies.

Skeletal Muscle: The skeletal muscle forms about 45% of the total weight of the body. About 0.5% muscle weight is due to glycogen content. Following a meal, the muscle glycogen content increases by about 1% of the total weight.

Muscle metabolism after a meal: The uptake and storage of glucose by the skeletal muscle is under the influence of insulin.

RELATED;

1.  Metabolism and metabolic disorders

2.  Biochemistry 

3.  Metabolism during starvation

REFERENCES

CITRIC ACID CYCLE

 

INTRODUCTION: The citric acid cycle,also known as the tricarboxylic acid (TCA) cycle or the Krebs cycle is a series of chemical reactions used by all aerobic organisms to generate energy through the oxidation of acetyl-CoA derived from carbohydrates, fats and proteins into carbon dioxide and chemical energy in the form of guanosine triphosphate (GTP)[carbohydrates] [proteins] [carbondioxide] [nucleotides] 

In addition, the cycle provides precursors of certain amino acids as well as the reducing agent NADH that is used in numerous other biochemical reactions. Its central importance to many biochemical pathways suggests that it was one of the earliest established components of cellular metabolism and may have originated a biogenically. 

[metabolism] [metabolic disorders]  

The citric acid cycle is a key metabolic pathway that unifies carbohydrate, fat, and protein metabolism. The reactions of the cycle are carried out by 8 enzymes that completely oxidize acetate, in the form of acetyl-CoA, into two molecules each of carbon dioxide and water. 

Through catabolism of sugars, fats, and proteins, a two-carbon organic product acetate in the form of acetyl-CoA is produced which enters the citric acid cycle.  The reactions of the cycle also convert three equivalents of nicotinamide adenine dinucleotide (NAD+) into three equivalents of reduced NAD+ (NADH), one equivalent of flavin adenine dinucleotide (FAD) into one equivalent of FADH2, and one equivalent each of guanosine diphosphate (GDP) and inorganic phosphate (Pi) into one equivalent of guanosine triphosphate (GTP). 

The NADH and FADH2 generated by the citric acid cycle are in turn used by the oxidative phosphorylation pathway to generate energy-rich adenosine triphosphate (ATP). [ATP]  

One of the primary sources of acetyl-CoA is from the breakdown of sugars by glycolysis which yield pyruvate that in turn is decarboxylated by the enzyme pyruvate dehydrogenase generating acetyl-CoA according to the following reaction scheme:

Pyruvate + CoASH + NAD+→ Acetyl-CoA + NADH + CO2

The product of this reaction, acetyl-CoA, is the starting point for the citric acid cycle. Acetyl-CoA may also be obtained from the oxidation of fatty acids. Below is a schematic outline of the cycle: 

(1) The citric acid cycle begins with the transfer of a two-carbon acetyl group from acetyl-CoA to the four-carbon acceptor compound (oxaloacetate) to form a six-carbon compound (citrate). 

(2) The citrate then goes through a series of chemical transformations, losing two carboxyl groups as CO₂. The carbons lost as CO₂ originate from what was oxaloacetate, not directly from acetyl-CoA. The carbons donated by acetyl-CoA become part of the oxaloacetate carbon backbone after the first turn of the citric acid cycle. Loss of the acetyl-CoA-donated carbons as CO₂ requires several turns of the citric acid cycle. However, because of the role of the citric acid cycle in anabolism, they might not be lost, since many TCA cycle intermediates are also used as precursors for the biosynthesis of other molecules. 

(3) Most of the energy made available by the oxidative steps of the cycle is transferred as energy-rich electrons to NAD+, forming NADH. For each acetyl group that enters the citric acid cycle, three molecules of NADH are produced. 

(4) Electrons are also transferred to the electron acceptor Q, forming QH₂. 

(5) At the end of each cycle, the four-carbon oxaloacetate has been regenerated, and the cycle continues.

RELATED;

1.  CARBOHYDRATES  

2.  GLUCAGON  

3.  GLYCOGEN

4.  BIOCHEMISTRY

REFERENCES

CHECKING FOR INSTALLED APPS IN ANDROID USING ADB COMMANDS

CHECKING FOR INSTALLED APPS IN ANDROID USING ADB COMMANDS:  There are many ways you can check for installed apps on android.  One way is through the phone settings but this route is not always the easiest for an average user and since these days the settings keeps on changing locations of different entries in different smartphones, the settings may not be the first choice for everyone. Also, there are time when apps are not seen on the smartphone but when they are actually installed.  One of the easiest way of seeing installed apps on your smartphone is by using adb commands.  I am one guy that have really liked using the adb commands and if you have not been following my blogs on adb, you can click here for full use of adb commands.

Requirements

1.  Minimal adb and Fastboot setup

Download Minimal adb and fastboot

2.  Original USB cable of the phone

3.  Smartphone USB drivers for your chipset

Download smartphone USB drivers

4.  A computer running windows

Steps

1.  Install Minimal adb and fastboot setup on your PC and then the smartphone drivers of your phone.

2.  Right click the minimal adb shortcut on your desktop and choose to run as administrator.

3.  Connect the phone to the PC via USB cable.  Make sure USB debugging is activated on your phone.  If you have issues activating USB debugging, you can click here for directions.

4.  Go back to the PC and on the Minimal adb interface enter the commands one by one

-adb devices

This command will show you whether you phone is detected.

-adb shell pm list packages

This command will display all the apps packages of installed apps on your smartphone

Conclusion:  The adb is a very useful tool to control your android smartphone.

RELATED;

1.  FULL LIST OF ADB COMMANDS

2.  HOW TO UNINSTALL ANDROID APPS USING ADB COMMANDS

THE ACTIONS OF GLUCAGON AND INSULIN

 

Introduction: Glucagon is a peptide hormone, and is one of the hormones produced by α cells of the pancreas from one of the divisions known as the endocrine pancreas.  Glucagon works to raise the concentration of glucose in the bloodstream from the liver and skeletal muscles, as the opposite step accomplished by Insulin, which lowers the glucose levels in blood and initiates it's storage for later use. 

Mechanism of Glucagon production:  The pancreas releases glucagon when the concentration of glucose in the bloodstream falls too low to sustain cellular respiration. This is especially true between meals, or during starvation.  Glucagon causes the liver to convert stored glycogen into glucose, which is released into the bloodstream in situations of lower than normal blood glucose. 

In a negative feedback mechanism, high blood-glucose levels stimulate the release of insulin from the endocrine pancreas. 

[glycogen] [insulin] [glucose] [carbohydrates] [negative feedback mechanism]  

Insulin:  Insulin allows glucose to be taken up and used by insulin-dependent tissues. Thus, glucagon and insulin are part of a feedback system that keeps blood glucose levels at a stable level. It increases energy expenditure and is elevated under conditions of stress. Glucagon generally elevates the concentration of glucose in the blood by promoting gluconeogenesis and glycogenolysis. 

[gluconeogenesis] 

Storage and release of Glucose:  Glucose is stored in the liver in the form of the polysaccharide glycogen, which is a glucan, which is a polymer made up of glucose molecules. Liver cells also known as hepatocytes, have glucagon receptors. When glucagon binds to the glucagon receptors, the liver cells convert the glycogen into individual glucose molecules and release them into the bloodstream, in a process known as glycogenolysis. 

As these stores become depleted, glucagon then encourages the liver and kidney to synthesize additional glucose by gluconeogenesis. Glucagon turns off glycolysis in the liver, causing glycolytic intermediates to be shuttled to gluconeogenesis. Glucagon also regulates the rate of glucose production through lipolysis. Glucagon induces lipolysis in humans under conditions of insulin suppression such as diabetes mellitus type 1.

RELATED;

1.  INSULIN  

2.  CARBOHYDRATES

3. THE ENDOCRINE PANCREAS

REFERENCES

RHEUMATOID ARTHRITIS

Introduction:  Rheumatoid arthritis (RA) is an inflammatory disorder of unknown origin that primarily involves the synovial membrane of the joints. Phagocytosis produces enzymes within the joint. The enzymes break down collagen, causing edema, proliferation of the synovial membrane, and ultimately pus formation. Pus destroys cartilage and erodes the bone. The consequence is loss of articular surfaces and joint motion.  Muscle fibers undergo degenerative changes. Tendon and ligament elasticity and contractile power are lost.

PREVALENCE:  RA affects 1% of the population worldwide, affecting women two to four times more often than men.

CLINICAL MANIFESTATIONS:  Clinical features are determined by the stage and severity of the disease.  Joint pain, swelling, warmth, erythema, and lack of function are classic symptoms.  Palpation of joints reveals spongy or boggy tissue. Fluid can usually be aspirated from the inflamed joint.

CHARACTERISTIC PATTERN OF JOINT INVOLVEMENT:  Begins with small joints in hands, wrists, and feet.  Progressively involves knees, shoulders, hips, elbows, ankles, cervical spine, and temporomandibular joints.  Symptoms are usually acute in onset, bilateral, and symmetric.  Joints may be hot, swollen, and painful; joint stiffness often occurs in the morning.  Deformities of the hands and feet can result from misalignment and immobilization.

EXTRAARTICULAR FEATURES:  Fever, weight loss, fatigue, anemia, sensory changes, and lymph node enlargement.  Raynaud’s phenomenon (cold- and stress-induced vasospasm).  Rheumatoid nodules, nontender and movable; found in subcutaneous tissue over bony prominences.  Arteritis, neuropathy, scleritis, pericarditis, splenomegaly, and Sjögren syndrome (dry eyes and mucous membranes)

ASSESSMENT AND DIAGNOSTIC METHODS: Several factors contribute to an RA diagnosis: rheumatoid nodules, joint inflammation detected on palpation, laboratory findings, extra-articular changes.  Rheumatoid factor is present in about three fourths of patients.  RBC count and C4 complement component are decreased; erythrocyte sedimentation rate is elevated.  C-reactive protein and antinuclear antibody test results may be positive.  Arthrocentesis and x-rays may be performed.

MEDICAL MANAGEMENT:  Treatment begins with education, a balance of rest and exercise, and referral to community agencies for support. Early RA: medication management involves therapeutic doses of salicylates or NSAIDs; includes new COX-2 enzyme blockers, antimalarials, gold, penicillamine, or sulfasalazine; methotrexate; biologic response modififiers and tumor necrosis factor-alpha (TNF) inhibitors are helpful; analgesic agents for periods of extreme pain. Moderate, erosive RA: formal program of occupational and physical therapy; an immunosuppressant such as cyclosporine may be added.  Persistent, erosive RA: reconstructive surgery and corticosteroids. Advanced unremitting RA: immunosuppressive agents such as methotrexate, cyclophosphamide, azathioprine, and leflunomide (highly toxic, can cause bone marrow suppression, anemia, GI tract disturbances, and rashes).  RA patients frequently experience anorexia, weight loss, and anemia, requiring careful dietary history to identify usual eating habits and food preferences. Corticosteroids may stimulate appetite and cause weight gain. Low-dose antidepressant medications (amitriptyline) are used to reestablish adequate sleep pattern and manage pain.

RELATED; 

1.  MEDICINE AND SURGERY

REFERENCES