۱۳۸۸ خرداد ۶, چهارشنبه
۱۳۸۸ اردیبهشت ۲۷, یکشنبه
۱۳۸۸ اردیبهشت ۱۸, جمعه
مصرف مقادير حساب شده مواد قندي در افراد مبتلا به ديابت (نوع 1 يا 2) تأثير منفي بر روي کنترل ديابت آنها نخواهد داشت. با اين وجود شيرين کننده هاي رژيمي نيز مي تواند جايگزيني مناسب در افرادي باشند که مصرف شيريني جات در آنها بالاست (مخصوصاً کودکان).
» انواع شيرين کننده هاي رژيمي
شيرين کننده هاي رژيمي به دو دسته " کالري زا" و "غير کالري زا" تقسيم مي شوند.
» شيرين کننده هاي کالري زا
دسته اول که شامل "فروکتوز"، "سوربيتول" و "مانيتول" مي باشند، حاوي کالري هستند و بنابراين مصرف آنها بايد حساب شده باشد تا منجر به اضافه وزن نگردد. همچنين مصرف زياد سوربيتول و مانيتول به علت عدم جذب کامل ددر روده ها موجب اسهال مي گردد.
بنابراين قبل از مصرف فرآورده هاي غذايي رژيمي به برچسب روي آنها که بيانگر ترکيباتشان است دقت کنيد. به طور کلي مصرف اين نوع شيرين کننده ها در افراد ديابتي چاق که داراي چربي خون بالايي نيز هستند، توصيه نمي شود.
» شيرين کننده هاي غير کالري زا
شيرين کننده هاي غير کالري زا مانند" ساخارين" و "آسپارتام" داراي هيچ کالري نيستند و باعث اضافه وزن نيز مي شوند. قدرت شيرين کنندگي آنها بسيار بيشتر از شکر معمولي مي باشد (حدود 200 برابر ). بعضي از اين شيرين کننده ها مثل آسپارتام در اثر حرارت زياد اثر شيرين کنندگي خود را از دست مي دهند و بنابراين نمي توان از آنها در کيک پزي استفاده کرد. همچنين مصرف زياد ساخارين در بعضي از حيوانات منجر به سرطان مثانه شده که البته هنوز در مورد انساني به اثبات نرسيده است. زنان باردار نيز بهتر است از ساخارين استفاده نکنند.
موارد مصرف: کلوتريمازول در درمانکانديدياز ناشي از کانديدا آلبيکنس و سايرگونههاي کانديدا، کچلي بدن و ران و پاناشي از تريکوفيتون روبروم، تريکوفيتونمنتاگروفيس، اپيدرموفيتون فلوکوزوم وميکروسپوروم کانيس، تيناورسيکالر(ناشي از پيتيروسپوروم)، اريپکولار(مالاسزيا فورفور) و در درمان عفونتقارچي اطراف ناخن و کچلي ريش و سرمصرف ميشود.
مکانيسم اثر: کلوتريمازول ساختارگوسترول را مهار کرده و با آسيبرساندن به غشاء سلولي قارچ و تغيير درنفوذپذيري آن، باعث خروج عناصرضروري داخل سلولي ميگردد. اين داروهمچنين ساخت تريگليسيريدها وفسفوليپيدها را توسط قارچ مهار ميکند.کلوتريمازول باعث افزايش غلظتهيدروژن پراکسايد داخل سلول قارچ شدهکه باعث نکروز سلولي و از بين رفتنعناصر داخل سلولي ميشود. اين دارومانع تبديل بلاستوسپورها به شکل ميسليفعال در کانديدا آلبيکنس ميشود.
فارماکوکينتيک کلوتريمازول: جذب سيستميک اين داروبعد از مصرف پوستي کم است ولي بعد ازمصرف از راه مهبل به ميزان 10 ـ 3 درصدجذب ميشود.
هشدارها: از تماس دارو با چشم خودداريشود.
نکات قابل توصيه: 1 ـ رعايت نکات بهداشتيمانند استفاده از لباس زيرنخي و يا استفادهاز کاندوم در هنگام آمیزش جنسی به درمان کمکميکند. 2 ـ در صورت مصرف دارو براي درمانکانديدياز، از بهکار بردن پانسمان بسته درموضع خودداري شود. 3 ـ در صورت عدم پاسخ به درمان بعد ازاطمينان از عدم وجود ساير پاتوژنها، دورهدرمان ممکن است مجددا تکرار شود.
مقدار مصرف: موضعي ـ روزي 2 بار صبحو عصر از محلول يا کرم بر روي موضعماليده شود.
قرص واژينال ـ در بيماران غير حامله200mg/day ترجيلا قبل از خواب به مدت3 روز يا 100mg/day به مدت 7 روزاستعمال ميگردد.
کرم واژينال ـ مقدار 50mg/day يکاپليکاتور از کرم يک درصدترجيحا قبل ازخواب به مدت 14 ـ 6 روز استعمالميشود.
Topical Cream: 1%
Topical Solution: 1%
Vaginal Cream: 1%
Vaginal Tablet: 100mg
۱۳۸۸ اردیبهشت ۱۴, دوشنبه
In cell biology, peroxisome proliferator-activated receptors (PPARs) are a group of nuclear receptor isoforms that exist across biology. They are intimately connected to cellular metabolism (carbohydrate, lipid and protein) and cell differentiation. They are transcription factors.NomenclatureThree types of PPARs have been identified: alpha, gamma and delta (beta).
α (alpha) - expressed in liver, kidney, heart, muscle, adipose tissue, and others.
γ (gamma) - although transcribed by the same gene, this PPAR exists in three forms:
γ1 - expressed in virtually all tissues, including heart, muscle, colon, kidney, pancreas and spleen.
γ2 - expressed mainly in adipose tissue (30 amino acids longer)
γ3 - expressed in macrophages, large intestine, white adipose tissue.
δ (delta) - expressed in many tissues but markedly in brain, adipose tissue and skin.
PPARs were originally identified in Xenopus frogs as receptors that induce the proliferation of peroxisomes in cells. The first PPAR (PPARα) was discovered during the search of a molecular target for a group of agents then referred to as "peroxisome proliferators", as they increased peroxisomes in rodent liver tissue, apart from improving insulin sensitivity. These agents, pharmacologically related to the fibrates were discovered in the early 1980s. When it turned out that PPARs played a much more versatile role in biology, the agents were in turn termed "PPAR ligands". The best-known PPAR ligands are the thiazolidinediones
What happened to PPARβ
After PPARδ (delta) was identified in humans in 1992, it turned out to be closely-related to the PPARβ (beta) previously described during the same year in other animals (Xenopus). The name PPARδ is generally used in the US whereas the use of the PPARβ denomination has remained in Europe where this receptor was initially discovered in Xenopus.Physiological function
All PPARs dimerize with the retinoid X receptor (RXR) and bind to specific regions on the DNA of target genes. These DNA sequences are termed PPREs (peroxisome proliferator response elements). The DNA consensus sequence is AGGTCAXAGGTCA with X being a random nucleotide. Generally, this sequence occurs in the promotor region of a gene, and when the PPAR binds its ligand, transcription of targets genes are increased or decreased, depending on the gene. The RXR also forms a heterodimer with a number of other receptors: the vitamin D receptor and the thyroid hormone receptor.PPAR-gamma Activation in the Fat Cell
The function of PPARs is modified by the exact shape of their ligand-binding domain (see below) and by a number of co-activators and co-repressors, the presence of which can stimulate or inhibit receptor function.
The ligands for the PPARs are free fatty acids and eicosanoids. PPARγ is activated by PGJ2 (a prostaglandin). In contrast, PPARα is activated by leukotriene B4.PPAR-delta Activation in the Muscle CellGeneticsThe three main forms are transcribed from different genes:
PPARα - chromosome 22q12-13.1 (OMIM 170998).
PPARγ - chromosome 3p25 (OMIM 601487).
PPARδ - chromosome 6p21.2-21.1 (OMIM 600409).
Hereditary disorders of all PPARs have been described, generally leading to a loss in function and concomitant lipodystrophy, insulin resistance and/or acanthosis nigricans. Of PPARγ, a gain-of-function mutation has been described and studied (Pro12Ala) which decreased the risk of insulin resistance; it is quite prevalent (allele frequency 0.03 - 0.12 in some populations). In contrast, pro115gln is associated with obesity. Some other polymorphisms have high incidence in populations with elevated body mass indexes.Structure
All PPARs have a basic structure of functional domains. The most important ones are the DBD (DNA binding domain) and the LBD (ligand binding domain). The DBD contains two zinc finger patterns which bind to the regulator region of DNA when the receptor is activated. The LBD has an extensive secondary structure of several alpha helices (13) and a beta sheet. Natural and synthetic ligands bind to the LBD, activating the receptor.Pharmacology and PPAR modulators
PPARα and PPARγ are the targets of a number of known medications and are under continuing research for other forms of pharmacological modulation. Muraglitazar and tesaglitazar, both experimental compounds, binds to both PPAR-alpha and PPAR-gamma.PPAR-alpha modulators
PPAR-alpha is the main target of fibrate drugs, a class of amphipathic carboxylic acids (clofibrate, gemfibrozil, ciprofibrate, bezafibrate and fenofibrate). They are used in cholesterol disorders (generally as an adjunctive to statins) and disorders that feature high triglycerides.
PPAR-gamma is the main target of the drug class of thiazolidinediones (TZDs), used in diabetes mellitus and other diseases that feature insulin resistance. It is also mildly activated by certain NSAIDs (such as ibuprofen) and indoles. Known inhibitors include the experimental agent GW-9662.
The H1N1 form of swine flu is one of the descendants of the Spanish flu that caused a devastating pandemic in humans in 1918–1919.As well as persisting in pigs, the descendants of the 1918 virus have also circulated in humans through the 20th century, contributing to the normal seasonal epidemics of influenza. However, direct transmission from pigs to humans is rare, with 12 cases in the U.S. since 2005.
The flu virus is perhaps the trickiest known to medical science; it constantly changes form to elude the protective antibodies that the body has developed in response to previous exposures to influenza or to influenza vaccines. Every two or three years the virus undergoes minor changes. Then, at intervals of roughly a decade, after the bulk of the world's population has developed some level of resistance to these minor changes, it undergoes a major shift that enables it to tear off on yet another pandemic sweep around the world, infecting hundreds of millions of people who suddenly find their antibody defenses outflanked. Even during the Spanish flu pandemic, the initial wave of the disease was relatively mild, while the second wave was highly lethal.Classification
SIV strains isolated to date have been classified either as Influenzavirus C or one of the various subtypes of the genus Influenzavirus A.
Influenza ASwine influenza is known to be caused by influenza A subtypes H1N1,H1N2, H3N1, H3N2, and H2N3.In swine, three influenza A virus subtypes (H1N1, H3N2, and H1N2) are circulating throughout the world. In the United States, the H1N1 subtype was exclusively prevalent among swine populations before 1998; however, since late August 1998, H3N2 subtypes have been isolated from pigs. As of 2004, H3N2 virus isolates in US swine and turkey stocks were triple reassortants, containing genes from human (HA, NA, and PB1), swine (NS, NP, and M), and avian (PB2 and PA) lineages.
Signs and symptoms
According to the Centers for Disease Control and Prevention (CDC), in humans the symptoms of swine flu are similar to those of influenza and of influenza-like illness in general. Symptoms include fever, cough, sore throat, body aches, headache, chills and fatigue. The 2009 outbreak has shown an increased percentage of patients reporting diarrhea and vomiting.
Because these symptoms are not specific to swine flu, a differential diagnosis of probable swine flu requires not only symptoms but also a high likelihood of swine flu due to the person's recent history. For example, during the 2009 swine flu outbreak in the United States, CDC advised physicians to "consider swine influenza infection in the differential diagnosis of patients with acute febrile respiratory illness who have either been in contact with persons with confirmed swine flu, or who were in one of the five U.S. states that have reported swine flu cases or in Mexico during the 7 days preceding their illness onset." A diagnosis of confirmed swine flu requires laboratory testing of a respiratory sample (a simple nose and throat swab).
Prevention of spread in humans I
nfluenza spreads between humans through coughing or sneezing and people touching something with the virus on it and then touching their own nose or mouth. Swine flu cannot be spread by pork products, since the virus is not transmitted through food. The swine flu in humans is most contagious during the first five days of the illness although some people, most commonly children, can remain contagious for up to ten days. Diagnosis can be made by sending a specimen, collected during the first five days, to the CDC for analysis.
Recommendations to prevent spread of the virus among humans include using standard infection control against influenza. This includes frequent washing of hands with soap and water or with alcohol-based hand sanitizers, especially after being out in public.Although the current trivalent influenza vaccine is unlikely to provide protection against the new 2009 H1N1 strain, vaccines against the new strain are being developed and could be ready as early as June 2009.
Experts agree that hand-washing can help prevent viral infections, including ordinary influenza and the new swine flu virus. Influenza can spread in coughs or sneezes, but an increasing body of evidence shows little particles of virus can linger on tabletops, telephones and other surfaces and be transferred via the fingers to the mouth, nose or eyes. Alcohol-based gel or foam hand sanitizers work well to destroy viruses and bacteria. Anyone with flu-like symptoms such as a sudden fever, cough or muscle aches should stay away from work or public transportation and should see a doctor to be tested.
Social distancing is another tactic. It means staying away from other people who might be infected and can include avoiding large gatherings, spreading out a little at work, or perhaps staying home and lying low if an infection is spreading in a community.
PathophysiologyInfluenza viruses bind through hemagglutinin onto sialic acid sugars on the surfaces of epithelial cells; typically in the nose, throat and lungs of mammals and intestines of birds.Swine flu in humans
People who work with poultry and swine, especially people with intense exposures, are at increased risk of zoonotic infection with influenza virus endemic in these animals, and constitute a population of human hosts in which zoonosis and reassortment can co-occur. Transmission of influenza from swine to humans who work with swine was documented in a small surveillance study performed in 2004 at the University of Iowa. This study among others forms the basis of a recommendation that people whose jobs involve handling poultry and swine be the focus of increased public health surveillance. The 2009 swine flu outbreak is an apparent reassortment of several strains of influenza A virus subtype H1N1, including a strain endemic in humans and two strains endemic in pigs, as well as an avian influenza.
The CDC reports that the symptoms and transmission of the swine flu from human to human is much like that of seasonal flu. Common symptoms include fever, lethargy, lack of appetite and coughing, while runny nose, sore throat, nausea, vomiting and diarrhea have also been reported.
characterization found that the hemagglutinin (HA) gene was similar to that of swine flu viruses present in United States pigs since 1999, but the neuraminidase (NA) and matrix protein (M) genes resembled versions present in European swine flu isolates. Viruses with this genetic makeup had not previously been found to be circulating in humans or pigs, but there is no formal national surveillance system to determine what viruses are circulating in pigs in the United States. The origins of this new strain remain unknown.
The earliest known human case, 5 year old Edgar Hernandez, was near a pig farm in La Gloria, Veracruz state, Mexico, that raises almost 1 million pigs a year. Residents of La Gloria have long complained about the clouds of flies that are drawn to the so-called 'manure lagoons' created by such mega-farms. Edgar Hernandez was thought to be suffering from ordinary influenza but laboratory testing revealed he had contracted swine flu. The boy went on to make a full recovery.Swine influenza. (2009, April 30). In Wikipedia, The Free Encyclopedia. Retrieved 10:05, April 30, 2009