Saturday, April 18, 2015

Cell Biology




                                                               Rho family of GTPases


                 The Rho family of GTPases is a family of small (21 kDa) signaling G protein, and is a subfamily of the Ras superfamily. The members of the Rho GTPase family have been shown to regulate many aspects of intracellular actin dynamics, and are found in all eukaryotic kingdoms, including yeasts and some plants. Three members of the family have been studied in detail: Cdc42, Rac1, and Rh0A. All G proteins are "molecular switches", and Rho proteins play a role in organelle development, cytoskeleton dynamics, cell movement, and other common cellular functions.





Friday, April 17, 2015

Cell Biology

                     



                                            Intrinsic apoptotic pathway

         The intrinsic signaling pathway for programmed cell death involves non-receptor–mediated intracellular signals, inducing activities in the mitochondria that initiate apoptosis.
Stimuli for the intrinsic pathway include viral infections or damage to the cell by toxins, free radicals, or radiation. Damage to the cellular DNA can also induce the activation of the intrinsic pathway for programmed cell death. These stimuli induce changes in the inner mitochondrial membrane that result in the loss of transmembrane potential, causing the release of pro-apoptotic proteins into the cytosol.
Pro-apoptotic proteins activate caspases that mediate the destruction of the cell through many pathways. These proteins also translocate into the cellular nucleus, inducing DNA fragmentation, a hallmark of apoptosis.
The regulation of pro-apoptotic events in the mitochondria occurs through activity of members of the Bcl-2 family of proteins and the tumor suppressor protein p53. Members of the Bcl-2 family of proteins may be pro- or anti-apoptotic7
The anti-apoptotic proteins are Bcl-2, Bcl-x, Bcl-xL, Bcl-XS, Bcl-w, and BAG. Some of these proteins are currently under investigation as potential targets for anticancertherapy.
Pro-apoptotic proteins include Bcl-10, Bax, Bak, Bid, Bad, Bim, Bik, and Blk. It has been suggested that upregulation of these proteins or their increased activation may offer an approach for cancer therapy.Cellular pathways that modulate the activities of the p53 protein are also currently being evaluated as targets for potential anticancer therapies.

Elements of the intrinsic apoptosis pathway image 

Cell Biology




                                                               MPF regulation

                       Cyclin-CDK (cyclin-dependent protein kinase) complexes play a central role in cell cycle progression . The function of cyclin-CDKs is to run the cell cycle smoothly, and these are therefore called “cell cycle engines.” Cyclins are proteins that vary in quantity throughout the cell cycle. The cyclins are expressed between the G1 and S phases, during the S phase, and between the G2 and M phases, known as the G1/S-phase cyclin, the S-phase cyclin, and the G2/M-phase cyclin, respectively. Each cyclin is rapidly synthesized during a specific phase of the cell cycle and is again promptly broken down after it serves its purpose. They are broken down not only because they are no longer needed, but because the breakdown is required for the cell cycle to transition to the next step. Meanwhile, the CDKs need to be synthesized de novo when cell proliferation starts from the G0 phase. Once the cell cycle starts, some types of CDK are broken down during a specific phase of the cell cycle, whereas others are not. When the cyclins and CDKs that are expressed in a specific phase are bonded and activated, they phosphorylate the specific serine and threonine residues of a target protein. The phosphorylated target protein executes the events occurring in the respective phases of the cell cycle.

Cell cycle control by cyclin-CDK

Microbiology





                                                               Salmonellosis

                          Salmonella infection is usually caused by eating raw or undercooked meat, poultry, eggs or egg products. The incubation period ranges from several hours to two days. Most salmonella infections can be classified as gastroenteritis. Possible signs and symptoms include:

Nausea
Vomiting
Abdominal cramps
Diarrhea
Fever
Chills
Headache
Blood in the stool
           Signs and symptoms of salmonella infection generally last four to seven days, although it may take several months for your bowels to return to normal.
Salmonella bacteria live in the intestines of people, animals and birds. Most people are infected with salmonella by eating foods that have been contaminated by feces. Commonly infected foods include:
·         Raw meat, poultry and seafood. 
·          Raw eggs. 
·          Fruits and vegetables.  



Persistent bacterial infections: the interface of the pathogen and the host immune system

Microbiology




                                               Hemolytic disease of the newborn


                     Hemolytic disease of the fetus and newborn (HDFN), erythroblastosis fetalis, is a blood disorder that occurs when the blood types of a mother and baby are incompatible.
The mother produces substances called antibodies that attack the developing baby's red blood cells.
                    The most common form of HDN is ABO incompatibility, which is usually not very severe. Other, less common types may cause more severe problems.
                   The least common form is Rh incompatibility, which can almost always be prevented. When this form does occur, it can cause very severe anemia in the baby.
HDN can destroy the newborn baby's blood cells very quickly, which can cause symptoms such as:

                         Edema (swelling under the surface of the skin)
·                                                             Newborn jaundice
    Signs of HDN include:
  • Anemia or low blood count
  • Enlarged liver or spleen
  • Hydrops that can lead to heart failure from too much fluid.

Microbiology





                              Methods of Detection of Hypersensitivity Reactions
 
                  Hypersensitivity reactions are classified into four groups: Type I, II, III, and IV, each         characterized by specific biological actions.
          Type I hypersensitivities can be determined by provacation testing, immediate-type skin testing, or radioallergosorbent tests (RASTs); Type II hypersensitivities can be determined by measuring the level of IgG antibodies to specific host proteins; Type III hypersensitivities may be detected with serum IgG antibody testing to specific antigens; Type IV hypersensitivities are determined by delayed skin testing or memory lymphocyte immunostimulation assay (MELISA).






Sunday, March 29, 2015

Cell Biology

                                                  

                                                 Vohwinkel syndrome

            vohwinkel syndrome is a disorder with classic and variant forms, both of which affect the skin.
             The classic form of Vohwinkel syndrome is caused by mutations in the GJB2 gene. This gene provides instructions for making a protein called gap junction beta 2, more commonly known as connexin 26. Connexin 26 is a member of the connexin protein family. Connexin proteins form channels called gap junctions that permit the transport of nutrients, charged atoms (ions), and signaling molecules between neighboring cells that are in contact with each other. Gap junctions made with connexin 26 transport potassium ions and certain small molecules.
           Connexin 26 is found in cells throughout the body, including the inner ear and the skin. In the inner ear, channels made from connexin 26 are found in a snail-shaped structure called the cochlea. These channels may help to maintain the proper level of potassium ions required for the conversion of sound waves to electrical nerve impulses. This conversion is essential for normal hearing. In addition, connexin 26 may be involved in the maturation of certain cells in the cochlea. Connexin 26 also plays a role in the growth, maturation, and stability of the outermost layer of skin (the epidermis).
             The GJB2 gene mutations that cause Vohwinkel syndrome change single protein building blocks (amino acids) in connexin 26. The altered protein probably disrupts the function of normal connexin 26 in cells, and may interfere with the function of other connexin proteins. This disruption could affect skin growth and also impair hearing by disturbing the conversion of sound waves to nerve impulses.