Inacio dos Santos

My dream to be a doctor now is on the way to achieve it and hope everything goes well till the end of my dream.


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Posted by IDS PHARMACY on January 22, 2013 at 7:45 AM Comments comments (0)

Microbose or Microorganisms are the organisms that cannot be seen by the naked eye, and only we can see by aided of the microscope, and these organisms that are caused diseases to the human beings or other mamal. 

The simplest definition of a microbe is a living thing, or ORGANISM, too tiny to be seen without the aid of a microscope. Most-but not all- are single cell (e.g. fungi are not single cell). Some, such as viruses are even "submicroscopic" requiring special electron microscopes to see them. Microbes fall into seven groups: bacteria, archaea, fungi, protists, microscopic animals, microscopic plants, and viruses. Although not all scientists agree that viruses should be included in the grouping, others do, for ease of discussion, even though they do not strictly meet the definition of microbes because they are not living. Viruses are organisms with specific behaviors and functions and the ability to reproduce or replicate, but they are particles rather than living microscopic organisms.



Posted by IDS PHARMACY on July 21, 2012 at 3:50 PM Comments comments (0)

Innate immunity is a host defense system with an immense repertoire of cellular and humoral components ranging from the skin as a physical barrier to serum proteins that possess highly specific recognition sites for molecular structures common to pathogens. This chapter reviews several major constituents of innate immunity and emphasizes the basic concept recognized by Janeway in 1989, that the innate immune system is critical for turning on the adaptive response (1). Absolutely necessary for effective inflammatory and humoral responses against external  pathogens, the innate immune system also seems to guard against autoreactivity and thus protects against autoimmune disease. Innate immunity's involvement during inflammation is discussed, and  omplement's role in humoral responses and in tolerance is reviewed to illustrate the linkages between the innate and adaptive immune systems.
In general, the innate immune system consists of three major components: (a) phagocytic cells, which eliminate microorganisms by ingesting and degrading them; (b) soluble plasma proteins and glycoproteins that bind microorganisms and target them for phagocytosis (i.e., opsonization) or for attack by the complement system, leading to microbial death by cytolysis; and (c) natural killer (NK) cells, a subset of primitive T cells pivotal for cell-mediated destruction of tumor cells and virally
infected cells. Detailed descriptions of each of these effector arms of innate immunity are provided in later chapters. In contrast to the adaptive immune system with its somatically rearranging, epitope-specific T- and B-cell receptors (TCRs and BCRs), components of the innate immune system do not mutate during the life of the host and do not exhibit memory when confronted with recurrent infections. Instead of somatic memory as defined by the adaptive immune system, the innate immune system has “evolutionary memory” with conserved components that recognize broad classes of molecules from common infectious agents. As a result, genetic deficiencies in various components of the innate immune system can have significant effects on the host's protective immune response.

Proper antigen recognition and handling comprise the crux of a normal immune system. Failure to recognize invading pathogens efficiently results in potentially lethal infections, and, conversely, unwarranted recognition of host-derived antigens may lead to autoimmune disease. The innate immune system ensures proper responses based on highly evolved cell-surface receptors and serum proteins that are specific for foreign structures and for self-structures. Many of the system's proteins actually recognize both foreign and host-derived cells and antigens. Because of the inherent risks in this dual recognition, the ability to reconcile mechanisms involved in innate recognition of cells and antigens may lead to novel strategies for both vaccine development and treatment of autoimmune disorders.
Components of the innate response recognize pathogen-associated molecular patterns (referred to as PAMPs) (2). The concept of pattern recognition is a relatively novel formulation of immune recognition. PAMPs include diverse moieties such as lipopolysaccharides (LPS) of gram-negative bacteria, peptidoglycans and lipoteichoic acid of gram-positive bacteria, and mannans of bacteria and fungi (1,3,4). PAMP recognition receptors (PRRs) are similarly diverse. For example, mannan-binding lectin (MBL) is a multimeric serum protein with six carbohydrate recognition domains that bind mannan with relatively high avidity (5). Binding of MBL to pathogen surfaces can activate the complement cascade, resulting in both microbial opsonization to facilitate uptake by phagocytic cells and microbial lysis through complement's membrane attack complex. The mannan receptor is a membrane form of MBL expressed on the surface of mammalian macrophages. Engagement of this receptor directly promotes phagocytosis of the pathogen and subsequent release of  proinflammatory chemical mediators (5).
Toll-like receptors (TLRs) are another class of protective PRRs that were described initially in the fruit fly Drosophila melanogaster (6). Conserved through evolution, this complex system of receptors responding to distinct ligands includes at least seven Tlr-related genes in Drosophila and six in humans (7). TLRs are found on mammalian phagocytic cells such as macrophages and on accessory cells such as dendritic cells (DCs) that are important links to adaptive immunity (8). TLRs can bind polypeptide products of proteolytic cascades such as the kinin system, which are often activated during bacterial infection. In addition, TLRs can be activated by secondary innate receptors. For example, mammalian TLR4 is activated indirectly by bacterial LPS after LPS binds the cell-surface receptor CD14 (9). TLR4 activation then triggers activation and translocation of nuclear factor-kB (NF-kB) from the cytoplasm to the nucleus and results in expression of inflammatory cytokines such as tumor necrosis factor-a (TNF-a) and interleukin-1 (IL-1) (9). Currently, intense research is under way to characterize other TLRs and ligands.
The protective power of innate immunity is amplified by a large collection of antimicrobial serum proteins and their cognate cell-surface receptors such as the complement system. When activated, the complement cascade of sequential proteolytic events generates many bioactive peptide fragments (10,11). The C3compon ent, for example, is enzymatically degraded in a stepwise manner resulting in distinct products identified according to molecular size: C3a, C3b, iC3b, and C3d.
For each distinct split product there are one or more cell-surface receptors whose engagement can induce diverse effects on cells of both the innate and adaptive immune systems. Indeed, at least two of these receptors, CD21 and CD35, are discussed later as important links between innate and adaptive immunity.
Host cells protect against viral infection or neoplastic transformation by random and continuous sampling of local microenvironments. NK cells are important participants in this immune surveillance (14,15). Technically a subfamily of T lymphocytes, NK cells use “hard wired” recognition receptors rather than somatically rearranged antigen receptors and therefore are considered components of the innate immune system. Both inhibitory and activating receptors, collectively referred to as killer immunoglobulin-like receptors (KIRs), are differentially expressed on NK cells (16,17). NK cell inhibitory receptors recognize conserved regions of the major histocompatibility complex (MHC) class I proteins that are expressed on nearly all host cells (16,18). Host cells expressing these heterodimeric glycoproteins repress NK cell activity. Viral infection or neoplastic transformation can disrupt normal MHC class I expression, and the absence of recognizable MHC class I molecules on host cell surfaces releases the baseline NK cell inhibitory signals, thus permitting NK cell activation. Activating receptors on NK cells include CD2, CD16, and CD69.
Coordinate signaling through these receptors allows recognition and potentiates killing of tumor cells or virally infected cells either by direct cytotoxicity or by antibody-dependent cellular cytotoxicity (ADCC) . ADCC is yet another link between innate and adaptive responses during which NK cell cytotoxicity is triggered by the stimulatory Fc receptor FcgRIIIA and by the complement receptor CR3 (CD11b/CD1 after recognition of abnormal cells that are coated with antibody and complement fragments.
The task of continuous immune surveillance by the innate immune system is shared with the alternative pathway of serum complement. Although there are some specific activators of complement, the system exists in a state of perpetual low-level activation through the spontaneous conformational changes or “tickover” of C3 molecules (19). Activated C3 can bind covalently to nearly any surface in its vicinity. C3 attachment to acceptor sites on pathogens triggers rapid amplification of the complement cascade and elimination of those invaders. Host tissues cells are protected from spontaneous complement-mediated injury because host cells express C3 inhibitors. This family of receptors and serum proteins, referred to as regulators of complement activation (RCA) (20), bind activated C3 (C3b) and either block propagation of the complement cascade or cooperate with factor I to degrade the C3 moiety. These regulators include membrane cofactor (CD46), decay-activating factor (CD55), and the Crry receptor (20). Mice lacking the Crry receptor are not viable (21), a finding implying that inadequate inhibition of the complement cascade induces spontaneous injury and death to the fetus.

Inflammation is a major consequence of activating the innate immune system. Classically identified by the four symptoms of heat, rash, edema, and pain, inflammation is the rapid response to an infectious organism that can lead to direct lysis or uptake of pathogens by phagocytic cells within minutes to hours. Serum and cellular components together mediate the phenotype. For example, local activation of the complement system can stimulate mast cell release of proinflammatory cytokines such as TNF-a, chemical mediators such as histamine and a variety of proteases (22). Together, these agents promote dilation and increase permeability of local blood vessels. By upregulating selectins on local endothelial cells, histamine can initiate margination and rolling of circulating leukocytes (23). Additional mediators such as the leukotrienes and platelet-activating factor further enhance the inflammatory response by upregulating integrins and leukocyte influx into the local tissues (24).
Complete characterization of inflammation is not the intent of this introductory chapter. Instead, two animal models of inflammatory processes are presented as specific examples of how inflammation can be both protective and pathogenic to the host. The first example is cecal ligation and puncture (CLP), a model for acute septic peritonitis that includes the combined interaction of serum and cellular components in clearing a bacterial infection. The second example, ischemia reperfusion (IR) injury, is a condition in which the host's innate immune system is provoked to attack self-tissue and can result in death depending on the severity of the inflammatory response.
Acute Septic Peritonitis as a Model for Host Protection
CLP is a mast cell–dependent model of acute septic peritonitis that can progress to fulminant sepsis (25,26). In this surgical model, the cecum is ligated, it is punctured to release bacteria from the intestine, and then the peritoneum is reclosed. Within minutes, bacteria in the peritoneum activate the innate response beginning with mast cell degranulation that, in turn, promotes massive infiltration of neutrophils similar to a ruptured appendix. The innate immune system is essential for host protection because the adaptive response is too slow to be protective in this acute infection model. Nonetheless, mice deficient in serum immunoglobulin M (IgM) have more fulminant sepsis than normal mice undergoing CLP. Reconstitution of IgM-deficient animals with natural IgM from naive unimmunized donors affords some protection against the sepsis syndrome (27). This observation suggests that spontaneously produced natural antibody may be considered a soluble component that is shared between the innate and adaptive immune systems (see later, in the discussion of innate immunity-mediated control of adaptive responses).
Because of its pentameric structure, IgM is effective at binding to pathogens and activating the classical pathway of complement (28,29). Antigen binding induces a conformational change in the antibody that allows C1q binding and initiates the classical complement pathway cascade, with sequential activation of complement components (see chapter 26 for detail on complement pathways). Deficiency in C3 or C4 or in their receptors CD21/CD35 dramatically increases morbidity and mortality in the CLP model (30). The impaired activation of the classical pathway reduces survival by blocking bacteriolysis by the C5-C9 membrane attack complex and by diminishing activation of peritoneal mast cells. In the absence of complement activation, peritoneal mast cells do not recruit neutrophils to the peritoneum, thereby permitting bacteria to escape opsonophagocytosis.
In summary, the CLP model identifies some of the cellular and serum components of innate immunity that are required in protection from severe bacterial infection. Although mast cells express PRRs, costimulatory interactions from IgM natural antibody and the classical pathway of complement are also required for complete mast cell activation. In the absence of IgM, complement or complement receptors (CD21/CD35), neutrophil infiltration and clearance of bacteria from the peritoneum are impaired.

Disorders of the Thyroid Gland

Posted by IDS PHARMACY on July 14, 2012 at 4:40 AM Comments comments (0)

The thyroid gland, the largest endocrine organ, weighs about 20 g. It develops from an evagination in the base of the tongue at the foramen cecum and descends anterior to the larynx via the thyroglossal duct; the latter usually disappears or remains as the pyramidal lobe. Congenital anomalies result from persistence of the thyroglossal duct or abnormal descent of the thyroid gland.

1. Persistent thyroglossal duct anomalies. In some patients, the epithelium of the thyroglossal cyst may persist as a fistula or a blind-ended cyst usually located above the thyroid cartilage.

Thyroglossal duct cysts, however, may present as midline structures from the base of the tongue to the suprasternal notch. Excision of the fistula or cyst should include resection of the midsection of

the hyoid bone to avoid recurrence (Sistrunk operation). About 1% of thyroglossal duct cysts contain a focus of papillary thyroid cancer and about 25% of these patients have thyroid cancer elsewhere

in the thyroid gland. The thyroid may also fail to descend and may result in a sublingual thyroid gland. Some patients with sublingual thyroids are hypothyroid, and the thyroid tissue may become

calcified (Figure 1–1). The pyramidal lobe hypertrophies in patients with Graves’ disease, multinodular goiter, or Hashimoto’s thyroiditis and can usually be palpated in the central


Posted by IDS PHARMACY on March 5, 2011 at 11:40 PM Comments comments (1)

HIV?AIDS  Introduction

AIDS is the acronym for the incurable disease  acquired immunodeficiency virus (HIV). AIDS is caused by an infection with the  human immunodeficiency virus (HIV). Over time, HIV infection  destroys the helper T cells of the body's immune system, resulting in a critical deterioration of the immune system and the ability of the body to fight infection. Advanced HIV infection  is called AIDS.

AIDS is frequently a sexually transmitted disease. HIV which causes ADIS is most often passed from one person another during sexual contact that involves vaginal, oral, or anal sex. HIV can also be passed to another person through other means, such as through contact with blood or body fluids. This can occur through such processes as blood transfusions or sharing needles contaminated with HIV. HIV can also be passed from an infected mother to her baby during pregnancy, childbirth or breastfeeding.

Early infection with HIV often produces no symptoms. When there are symptoms, they can include flu - like symtoms  that occur about four to eight weeks after infection. These symptoms generally go away within several weeks. There then may be no symptoms for months to years. Eventually a person with HIV infection  develops serious, life-threatening complications. This is generally when a diagnosis of AIDS is made. For more details on complications and symptoms, refer to symptoms of AIDS.

Any person that engages in sexual activity can contract and pass on the HIV infection, which causes AIDS. This includes heterosexual, homosexual, and bisexual men and women. The more sexual partners a person has, the greater the risk of catching and passing on an HIV infection. Having another type of sexually transmitted disease, such as shlamydia, genetial herpes, HPV or gonorrhea, also puts a person at greater risk for contracting an HIV infection and eventually developing AIDS.

The diagnostic test for HIV is a blood test that can reveal the presence of the specific antibodies (infection-fighting substances) that the body makes in response to an HIV infection. However, HIV may not be detectable in the first one to three months after infection. A diagnosis of AIDS is generally made when HIV infection  has resulted in serious complications and opportunistic infections  are occurring. These can include  pneumocystis carinii pneumonia,  kaposi's sarcoma  and tuberculosis .

During or after a diagnosis of AIDS, a physician or licensed health care provider will take a medical and sexual history to determine general health and immune system status. A complete physical and pelvic examination  for women and physical and examination of the penis and testicles for men  is also done. Additional tests are done to test for the presence of other potential disorders and diseases, including sexually transmitted diseases.

Because there are often no symptoms in the early stages, some people with AIDS may be unaware of an HIV infection, and a diagnosis can be missed or delayed. For more information on misdiagnosis, refer to misdiagonosis of HIV.

AIDS is a highly preventable disease. Prevention of AIDS is best accomplished by abstaining from sexual activity or having sex only within a mutually monogamous relationship in which neither partner is infected with HIV. Latex  condoms  also provide some protection from HIV and AIDS when used properly.

There currently is no cure for HIV infection  and AIDS. However, prompt diagnosis and treatment of  HIV infection can help to delay the onset of AIDS and serious complications, such as opportunistic infections, improve the quality of life, and minimize the spread of the disease to others. Treatment generally includes medications. Hospitalization may be necessary if a person has serious complications, such as meningitis  or an opportunistic infection. For more information on treatment, refer to treament of AIDS . ..

AIDS: Acquired immune deficiency  syndrome (AIDS) is the result of an infection with the human immunodeficiency virus (HIV). This virus attacks selected cells of the ... 

AIDS: A term given to HIV patients who have a low CD4 count (below 200) which means that they have low levels of a type of immune cell called T-cells. AIDS patients tend to develop opportunistic infections symptoms, causes, and treatment of AIDS is available below. and cancers. Opportunistic infections are infections that would not normally affect a person with a healthy immune system. The HIV virus is a virus that attacks the body's immune system. More detailed information about the

Early Signs and Symptoms of HIV Some people experience signs and symptoms of HIV (Human Immunodeficiency Virus), as soon as they become infected, while others do not. When they occur, early signs and symptoms are often mistaken for the flu or a mild viral infection. Initial signs and symptoms of HIV include: FeverHeadacheTirednessNauseaDiarrheaEnlarged lymph nodes in the neck, armpits or groin Any symptoms from becoming infected typically resolve in one to four weeks.

As you can see, the signs and symptoms of HIV infection are similar to those for many different viral infections. The only way to know for sure if you are infected with HIV is to be tested. Many people infected with HIV do not have any signs and symptoms at all for many years.

Later Signs and Symptoms of HIV/AIDS The Centers for Disease Control (CDC) says the following signs and symptoms may be warning signs of late-stage HIV infection: rapid weight lossdry coughrecurring fever or profuse night sweatsprofound and unexplained fatigueswollen lymph glands in the armpits, groin, or neckdiarrhea lasting more than a weekwhite spots or unusual blemishes on the tongue, in the mouth, or in the throatpneumoniared, brown, pink, or purplish blotches on or under the skin or inside the mouth, nose, or eyelidsmemory loss, depression, and other neurological disorders HIV destroys the white blood cells that are required to fight infection. As the white cell count falls to dangerous levels, numerous infections and diseases emerge. It is at this point that a person is said to have AIDS (Acquired Immune Deficiency Syndrome).

According to the CDC, as with an initial HIV infection, you cannot rely on these signs and symptoms to establish a diagnosis of AIDS. The symptoms of AIDS are similar to the symptoms of many other illnesses. AIDS is a medical diagnosis made by a healthcare professional based on specific criteria established by the CDC.


the HIV/AIDS patients

the penis of HIV/Patient


Posted by IDS PHARMACY on November 29, 2010 at 6:13 AM Comments comments (0)



A biotechnology company asserted yesterday that it had made a significant advance toward artificially producing a blood substance needed by thousands of hemophiliacs to curb excessive bleeding.


Genetics Institute, a Boston-based company, said research led by Dr. Jay Toole ''has successfully cloned'' a substance representing the human gene for a protein that is defective or missing from the blood of people suffering from the most common form of hemophilia.


The cloned substance is deoxyribonucleic acid, or DNA, the active substance of the genes of all living things. The protein, is factor VIII, which is defective or missing in people with hemophilia A, a form of the hereditary blood disorder that inhibits natural clotting.


The cloning of a piece of DNA means that it has been obtained in pure form and can be produced in large quantity in bacteria. Dr. Toole said his group had cloned a significant portion of the gene for human blood factor VIII, but did not yet have a full-length clone.


''To our knowledge this is the first time anyone has had a piece of the gene,'' said Dr. Toole. Step Toward Mass Production


At present, the substance is purified from human blood. Cloning DNA of the human gene is a step toward large-scale production of the blood substance itself in bacteria or other organisms such as yeast.


Dr. Toole and others not associated with his company emphasized, however, that such production was probably still years in the future. When it does become possible, artificial production in microbes should lead to a safer, cheaper and more plentiful supply of the blood factor.


Most of the 20,000 hemophiliacs in the United States take infusions of blood factor VIII about 30 to 50 times a year to cope with bleeding episodes. The total cost to such a patient ranges from $5,000 to $10,000, according to Alan Brownstein, executive director of the National Hemophilia Foundation.


Use of factor VIII from human blood carries some risk of infection, notably with the hepatitis B virus. That risk would be eliminated if the substance were produced by microbes. Good News' for Patients


Mr. Brownstein described the report from Boston as ''good news,'' although he said hemophilia patients should bear in mind that it might be several years before a new source of supply of the blood substance becomes available.


The research at Genetics Institute is sponsored by Hyland Therapeutics of Glendale, Calif., a division of Baxter Travenol Laboratories, Inc.


The announcement yesterday said: ''The success at Genetics Institute opens the way to the ultimate manufacture of pure factor VIII protein from genetically engineered organisms. The cloned DNA will also prove valuable as a research tool for studying the molecular basis of the disease which afflicts about one in 20,000 males.'' Hemophilia occurs in males, but is transmitted by females.


In a telephone interview, Dr. Toole said his company hoped to have human blood factor VIII available for tests in humans in about two years.


The substance has been difficult to study, he said, because it is present in human blood only in trace amounts and is not very stable chemically under laboratory conditions.


He said it was detected with the aid of a known gene for the comparable blood substance of pigs.



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