Steroid dependent minimal change disease

In effort to list a protocol for the use of GHRP / GRF / and in combo with GH if desired I thought I would post my current protocol based upon the research I have done within the last year or so. Obviously the information I gathered is not based on medical studies completed by me but I do use the following protocol myself and have been pretty damed impressed with the results. Recovery from injury is very impressive to me (any kind of injury). Example, 5 days ago I was lifted by the butt of a tree I cut down (long story). I had bruising and some serious raspberry on my under arm, left quad and my abs ( the but of the tree ran right up the front of my once it got under my arm it lifted me and tossed me about 10 feet through the air). Its been 5 days and all that is left of the raspberries are some faint red marks......amazing IMO.

This is the scenario: a guy, say age 21, becomes serious about gaining muscle. He’s 5′ 10″, 7″ wrists, 9″ ankles, average genetics for muscle size-and-proportioned. He’s played sports, but never done more than an occasional resistance workout. Now, he begins a good training-eating-and-resting program. With his genetics, he has the potential for naturally gaining 45 pounds of lean mass if he stays consistent with progressive training/proper eating for a continuous 3 to 4 years.
But, about three months after beginning his training, he starts taking steroids. He does three steroid cycles in the following 18 months, and includes proper post-cycle therapy. That entire time, he’s continuing to consistently train and eat properly. Before the end of two years, he’s gained 45 pounds of lean mass (which with steroids, by the way, is not necessarily typical but neither improbable). At that point, he permanently quits using steroids, but he does continue properly training and eating for another two years. At the end of four years, he carries the same 45 pounds of lean mass.

An acute myopathy has been observed with the use of high doses of corticosteroids, most often occurring in patients with disorders of neuromuscular transmission (., myasthenia gravis ), or in patients receiving concomitant therapy with neuromuscular blocking drugs (., pancuronium). This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis . Elevations of creatine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.

There are numerous classes of protein that span the membrane of cells, be it the plasma membrane or intracellular organellar membranes. The transmembrane proteins include the various ion channels, other types of channel proteins, transporter proteins, growth factor receptors, and cell adhesion molecules. All transmembrane proteins, regardless of function, are classified dependent upon their structure. There are four main classifications for transmembrane proteins, type I, II, III, and IV. Types I, II, and III are all characterized by passing through the membrane once, referred to as single-pass transmembrane proteins. Type IV transmembrane proteins pass through the membrane several times and, therefore, they are all referred to as multiple-pass transmembrane proteins. Type I transmembrane proteins are anchored to the membrane via a sequence of hydrophobic amino acids referred to as the stop-transfer sequence and this class all have the C-terminus of the protein inside the cell and the N-terminus outside. A typical example of a type I transmembrane protein is the LDL receptor . Type II transmembrane proteins are anchored to the membrane via a signal-anchor sequence and have the C-terminus outside the cell and the N-terminus inside. An example of a type II transmembrane protein is the transferrin receptor . Type III transmembrane proteins do not have a signal sequence and the N-terminus of the protein is outside the cell. An example of a type III transmembrane protein would be any member of the cytochrome P450 family of xenobiotic metabolizing enzymes found in the liver. Type IV transmembrane proteins are typified by the G-protein coupled receptor (GPCR) superfamily of receptor proteins that span the membrane seven times. This class of receptor is often referred to as the serpentine receptor family because of the multiple membrane spans. Another example of a type IV transmembrane protein is the α-subunit of a typical Na + ,K + -ATPase (see below). Type IV transmembrane proteins are divided into type IV-A and type IV-B where the IV-A members have the N-terminus inside the cell and the C-terminus outside and the IV-B members are oriented in the opposite direction. The Na + ,K + -ATPase α-subunit proteins are type IV-A multi-pass transmembrane proteins, whereas, all GPCRs are members of the type IV-B family.

Steroid dependent minimal change disease

steroid dependent minimal change disease

There are numerous classes of protein that span the membrane of cells, be it the plasma membrane or intracellular organellar membranes. The transmembrane proteins include the various ion channels, other types of channel proteins, transporter proteins, growth factor receptors, and cell adhesion molecules. All transmembrane proteins, regardless of function, are classified dependent upon their structure. There are four main classifications for transmembrane proteins, type I, II, III, and IV. Types I, II, and III are all characterized by passing through the membrane once, referred to as single-pass transmembrane proteins. Type IV transmembrane proteins pass through the membrane several times and, therefore, they are all referred to as multiple-pass transmembrane proteins. Type I transmembrane proteins are anchored to the membrane via a sequence of hydrophobic amino acids referred to as the stop-transfer sequence and this class all have the C-terminus of the protein inside the cell and the N-terminus outside. A typical example of a type I transmembrane protein is the LDL receptor . Type II transmembrane proteins are anchored to the membrane via a signal-anchor sequence and have the C-terminus outside the cell and the N-terminus inside. An example of a type II transmembrane protein is the transferrin receptor . Type III transmembrane proteins do not have a signal sequence and the N-terminus of the protein is outside the cell. An example of a type III transmembrane protein would be any member of the cytochrome P450 family of xenobiotic metabolizing enzymes found in the liver. Type IV transmembrane proteins are typified by the G-protein coupled receptor (GPCR) superfamily of receptor proteins that span the membrane seven times. This class of receptor is often referred to as the serpentine receptor family because of the multiple membrane spans. Another example of a type IV transmembrane protein is the α-subunit of a typical Na + ,K + -ATPase (see below). Type IV transmembrane proteins are divided into type IV-A and type IV-B where the IV-A members have the N-terminus inside the cell and the C-terminus outside and the IV-B members are oriented in the opposite direction. The Na + ,K + -ATPase α-subunit proteins are type IV-A multi-pass transmembrane proteins, whereas, all GPCRs are members of the type IV-B family.

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