Thursday, 18 December 2014
Pancreas & Cystic Fibrosis
Cystic fibrosis (CF), also known as mucoviscidosis, is an autosomal recessive genetic disorder that affects mostly the lungs but also the pancreas, liver, and intestine. Difficulty breathing is the most serious symptom and results from frequent lung infections. Other symptoms—including sinus infections, poor growth, and infertility—affect other parts of the body.
CF is caused by one of many different mutations in the gene for the protein cystic fibrosis transmembrane conductance regulator (CFTR). This protein is required to regulate the components of sweat, digestive fluids, and mucus. Healthy people have two working copies of the CFTR gene. Carriers have one working copy. People with CF have no working copy. CF therefore has autosomal recessive inheritance. The underlying mechanism is abnormal transport of chloride and sodium across the epithelium, which is the cell layer that covers membranes over organs. This leads to thick, viscous secretions. Individuals with cystic fibrosis can be diagnosed before birth by genetic testing or by a sweat test in early childhood.
Lung infections are treated with antibiotics and other medications. Ultimately, lung transplantation is often necessary as CF worsens. The average life expectancy is 37 to 40 years in the United States. CF is most common among people of Central and Northern European ancestry, but occurs in many different groups around the world. It is rarest among Asians and the Middle Easterns.
The name cystic fibrosis refers to the characteristic scarring (fibrosis) and cyst formation within the pancreas, first recognized in the 1930s
Parathyroid Hormone
Parathyroid hormone (PTH), parathormone or parathyrin, is secreted by the chief cells of the parathyroid glands as a polypeptide containing 84 amino acids. It acts to increase the concentration of calcium (Ca2+) in the blood, whereas calcitonin (a hormone produced by the parafollicular cells (C cells) of the thyroid gland) acts to decrease calcium concentration. 
PTH acts to increase the concentration of calcium in the blood by acting upon the parathyroid hormone 1 receptor (high levels in bone and kidney) and the parathyroid hormone 2 receptor (high levels in the central nervous system, pancreas, testis, and placenta). PTH half-life is approximately 4 minutes. It has a molecular mass of 9.4 kDa
PTH acts to increase the concentration of calcium in the blood by acting upon the parathyroid hormone 1 receptor (high levels in bone and kidney) and the parathyroid hormone 2 receptor (high levels in the central nervous system, pancreas, testis, and placenta). PTH half-life is approximately 4 minutes. It has a molecular mass of 9.4 kDaPenile Erection
An erection (clinically: penile erection or penile tumescence) is a physiological phenomenon in which the penis becomes firmer, engorged and enlarged. Penile erection is the result of a complex interaction of psychological, neural, vascular and endocrine factors, and is often associated with sexual arousal or sexual attraction, although erections can also be spontaneous. The shape, angle and direction of an erection varies considerably in humans.
Physiologically, erection is triggered by the parasympathetic division of the autonomic nervous system (ANS), causing nitric oxide (a vasodilator) levels to rise in the trabecular arteries and smooth muscle of the penis. The arteries dilate causing the corpora cavernosa of the penis (and to a lesser extent the corpora spongiosum) to fill with blood; simultaneously the ischiocavernosus and bulbospongiosus muscles compress the veins of the corpora cavernosa restricting the egress and circulation of this blood. Erection subsides when parasympathetic activity reduces to baseline.
As an autonomic nervous system response, an erection may result from a variety of stimuli, including sexual stimulation and sexual arousal, and is therefore not entirely under conscious control. Erections during sleep or upon waking up are known as nocturnal penile tumescence (NPT). Absence of nocturnal erection is commonly used to distinguish between physical and psychological causes of erectile dysfunction and impotence.
A penis which is partly, but not fully, erect is sometimes known as a semi-erection (clinically: partial tumescence); a penis which is not erect is typically referred to as being flaccid, or soft.
Physiologically, erection is triggered by the parasympathetic division of the autonomic nervous system (ANS), causing nitric oxide (a vasodilator) levels to rise in the trabecular arteries and smooth muscle of the penis. The arteries dilate causing the corpora cavernosa of the penis (and to a lesser extent the corpora spongiosum) to fill with blood; simultaneously the ischiocavernosus and bulbospongiosus muscles compress the veins of the corpora cavernosa restricting the egress and circulation of this blood. Erection subsides when parasympathetic activity reduces to baseline.
As an autonomic nervous system response, an erection may result from a variety of stimuli, including sexual stimulation and sexual arousal, and is therefore not entirely under conscious control. Erections during sleep or upon waking up are known as nocturnal penile tumescence (NPT). Absence of nocturnal erection is commonly used to distinguish between physical and psychological causes of erectile dysfunction and impotence.
A penis which is partly, but not fully, erect is sometimes known as a semi-erection (clinically: partial tumescence); a penis which is not erect is typically referred to as being flaccid, or soft.
Peptide Hormone Action
Peptide hormones are proteins that have an effect on the endocrine system of animals.
Like other proteins, peptide hormones are synthesized in cells from amino acids according to mRNA transcripts, which are synthesized from DNA templates inside the cell nucleus. Preprohormones, peptide hormone precursors, are then processed in several stages, typically in the endoplasmic reticulum, including removal of the N-terminal signal sequence and sometimes glycosylation, resulting in prohormones. The prohormones are then packaged into membrane-bound secretory vesicles, which can be secreted from the cell by exocytosis in response to specific stimuli (e.g. --an increase in Ca2+ and cAMP concentration in cytoplasm).
These prohormones often contain superfluous amino acid residues that were needed to direct folding of the hormone molecule into its active configuration but have no function once the hormone folds. Specific endopeptidases in the cell cleave the prohormone just before it is released into the bloodstream, generating the mature hormone form of the molecule. Mature peptide hormones then travel through the blood to all of the cells of the body, where they interact with specific receptors on the surfaces of their target cells. Some peptide/protein hormones (angiotensin II, basic fibroblast growth factor-2, parathyroid hormone-related protein) also interact with intracellular receptors located in the cytoplasm or nucleus by an intracrine mechanism.
Notable peptide hormones
Several important peptide hormones are secreted from the pituitary gland. The anterior pituitary secretes three: prolactin, which acts on the mammary gland; adrenocorticotropic hormone (ACTH), which acts on the adrenal cortex to regulate the secretion of glucocorticoids; and growth hormone, which acts on bone, muscle, and the liver. The posterior pituitary gland secretes antidiuretic hormone, also called vasopressin, and oxytocin. Peptide hormones are produced by many different organs and tissues, however, including the heart (atrial-natriuretic peptide (ANP) or atrial natriuretic factor (ANF)) and pancreas (glucagon, insulin and somatostatin), the gastrointestinal tract (cholecystokinin, gastrin), and adipose tissue stores (leptin).
Some neurotransmitters are secreted and released in a similar fashion to peptide hormones, and some 'neuropeptides' may be used as neurotransmitters in the nervous system in addition to acting as hormones when released into the blood. When a peptide hormone binds to receptors on the surface of the cell, a second messenger appears in the cytoplasm, which triggers intracellular responses
Photosynthesis Light Dependent
The light-dependent reactions take place on the thylakoid membranes. The inside of the thylakoid membrane is called the lumen, and outside the thylakoid membrane is the stroma, where the light-independent reactions take place. The thylakoid membrane contains some integral membrane protein complexes that catalyze the light reactions. There are four major protein complexes in the thylakoid membrane: Photosystem II (PSII), Cytochrome b6f complex, Photosystem I (PSI), and ATP synthase. These four complexes work together to ultimately create the products ATP and NADPH.
The two photosystems absorb light energy through pigments - primarily the chlorophylls, which are responsible for the green color of leaves. The light-dependent reactions begin in photosystem II. When a chlorophyll a molecule within the reaction center of PSII absorbs a photon, an electron in this molecule attains a higher energy level. Because this state of an electron is very unstable, the electron is transferred from one to another molecule creating a chain of redox reactions, called an electron transport chain (ETC). The electron flow goes from PSII to cytochrome b6f to PSI. In PSI, the electron gets the energy from another photon. The final electron acceptor is NADP. In oxygenic photosynthesis, the first electron donor is water, creating oxygen as a waste product. In anoxygenic photosynthesis various electron donors are used.
Cytochrome b6f and ATP synthase work together to create ATP. This process is called photophosphorylation, which occurs in two different ways. In non-cyclic photophosphorylation, cytochrome b6f uses the energy of electrons from PSII to pump protons from the stroma to the lumen. The proton gradient across the thylakoid membrane creates a proton-motive force, used by ATP synthase to form ATP. In cyclic photophosphorylation, cytochrome b6f uses the energy of electrons from not only PSII but also PSI to create more ATP and to stop the production of NADPH. Cyclic phosphorylation is important to create ATP and maintain NADPH in the right proportion for the light-independent reactions.
The net-reaction of all light-dependent reactions in oxygenic photosynthesis is:
2H
2O + 2NADP+
+ 3ADP + 3Pi → O
2 + 2NADPH + 3ATP
The two photosystems are protein complexes that absorb photons and are able to use this energy to create an electron transport chain. Photosystem I and II are very similar in structure and function. They use special proteins, called light-harvesting complexes, to absorb the photons with very high effectiveness. If a special pigment molecule in a photosynthetic reaction center absorbs a photon, an electron in this pigment attains the excited state and then is transferred to another molecule in the reaction center. This reaction, called photoinduced charge separation, is the start of the electron flow and is unique because it transforms light energy into chemical forms.
Phagocytic Cells
Phagocytic Cells
Phagocytes are cells that protect the body by ingesting (phagocytosing) harmful foreign particles, bacteria, and dead or dying cells. Their name comes from the Greek phagein, "to eat" or "devour", and "-cyte", the suffix in biology denoting "cell", from the Greek kutos, "hollow vessel". They are essential for fighting infections and for subsequent immunity. Phagocytes are important throughout the animal kingdom and are highly developed within vertebrates. One litre of human blood contains about six billion phagocytes. They were first discovered in 1882 by Ilya Ilyich Mechnikov while he was studying starfish larvae.Mechnikov was awarded the 1908 Nobel Prize in Physiology or Medicine for his discovery. Phagocytes occur in many species; some amoebae behave like macrophage phagocytes, which suggests that phagocytes appeared early in the evolution of life.
Phagocytes of humans and other animals are called "professional" or "non-professional" depending on how effective they are at phagocytosis.The professional phagocytes include many types of white blood cells (such as neutrophils, monocytes, macrophages, mast cells, and dendritic cells).The main difference between professional and non-professional phagocytes is that the professional phagocytes have molecules called receptors on their surfaces that can detect harmful objects, such as bacteria, that are not normally found in the body. Phagocytes are crucial in fighting infections, as well as in maintaining healthy tissues by removing dead and dying cells that have reached the end of their lifespan.
During an infection, chemical signals attract phagocytes to places where the pathogen has invaded the body. These chemicals may come from bacteria or from other phagocytes already present. The phagocytes move by a method called chemotaxis. When phagocytes come into contact with bacteria, the receptors on the phagocyte's surface will bind to them. This binding will lead to the engulfing of the bacteria by the phagocyte. Some phagocytes kill the ingested pathogen with oxidants and nitric oxide. After phagocytosis, macrophages and dendritic cells can also participate in antigen presentation, a process in which a phagocyte moves parts of the ingested material back to its surface. This material is then displayed to other cells of the immune system. Some phagocytes then travel to the body's lymph nodes and display the material to white blood cells called lymphocytes. This process is important in building immunity. However, many pathogens have evolved methods to evade attacks by phagocytes.
Phagocytes are cells that protect the body by ingesting (phagocytosing) harmful foreign particles, bacteria, and dead or dying cells. Their name comes from the Greek phagein, "to eat" or "devour", and "-cyte", the suffix in biology denoting "cell", from the Greek kutos, "hollow vessel". They are essential for fighting infections and for subsequent immunity. Phagocytes are important throughout the animal kingdom and are highly developed within vertebrates. One litre of human blood contains about six billion phagocytes. They were first discovered in 1882 by Ilya Ilyich Mechnikov while he was studying starfish larvae.Mechnikov was awarded the 1908 Nobel Prize in Physiology or Medicine for his discovery. Phagocytes occur in many species; some amoebae behave like macrophage phagocytes, which suggests that phagocytes appeared early in the evolution of life.
Phagocytes of humans and other animals are called "professional" or "non-professional" depending on how effective they are at phagocytosis.The professional phagocytes include many types of white blood cells (such as neutrophils, monocytes, macrophages, mast cells, and dendritic cells).The main difference between professional and non-professional phagocytes is that the professional phagocytes have molecules called receptors on their surfaces that can detect harmful objects, such as bacteria, that are not normally found in the body. Phagocytes are crucial in fighting infections, as well as in maintaining healthy tissues by removing dead and dying cells that have reached the end of their lifespan.
During an infection, chemical signals attract phagocytes to places where the pathogen has invaded the body. These chemicals may come from bacteria or from other phagocytes already present. The phagocytes move by a method called chemotaxis. When phagocytes come into contact with bacteria, the receptors on the phagocyte's surface will bind to them. This binding will lead to the engulfing of the bacteria by the phagocyte. Some phagocytes kill the ingested pathogen with oxidants and nitric oxide. After phagocytosis, macrophages and dendritic cells can also participate in antigen presentation, a process in which a phagocyte moves parts of the ingested material back to its surface. This material is then displayed to other cells of the immune system. Some phagocytes then travel to the body's lymph nodes and display the material to white blood cells called lymphocytes. This process is important in building immunity. However, many pathogens have evolved methods to evade attacks by phagocytes.
Subscribe to:
Posts (Atom)