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waitstay · 5 years ago

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Lundi confinement #6

Previously dans le coronavirus vu par Juju : notre aimée protagoniste allait un peu mieux après avoir eu à traverser quelques épreuves douloureuses.

Lundi : je n’ai absolument rien fait, même pas de sport pcq je déprimais. J’ai fait ma grosse drama queen et suis restée dans le noir toute la journée, j’ai rematté Euphoria, et à la fin j’ai décidé que ça suffit.

Mardi : aujourd’hui je devais aller à la pharmacie et faire 2/3 courses et j’ai croisé Fex *par hasard* (c’est une de mes meilleures amies, que j’insulte par messages si vous avez vu les posts). Il se peut que je lui ai dit “je serai à telle heure à tel endroit ;) ;)” donc on a fait nos courses ensemble et j’ai bien rigolé. Les potes me manquent beaucoup beaucoup.

Mercredi : j'ai pas été très productive. J'ai fait des dessins, j'ai décidé de rentrer dans une phase upgradée de ma sèche donc j'ai un peu la dalle mais je sais qu'en sèche la première semaine est toujours la plus dure. D'autant que vous le savez, j'ai très envie de frites. J’y pense tous les jours. Vous me manquez mes petits anges délicieux.

Jeudi : aujourd'hui j'ai encore rien fait (j'ai bu une bière et j'ai mangé des noix voilà ma sèche) donc je vais faire un point skincare. J'ai pas vraiment de l'acné en général mais j'ai eu une grosse phase boutons là + de l'eczéma (sur la même zone because why not) donc le matin je bois un thé chelou, je lave mon visage 2 fois par jour À L'EAU FROIDE, le matin je met une crème cicatrisante (j’ai oublié le nom, ça fait 3 fois que je regarde mon tube pour le renoter ici j’oublie à chaque fois, j’abandonne) et le soir je met un sérum de ma composition (huile de jojoba, huile de nigelle, huile essentielle de lavande vraie). Je suis toujours moche mais y'a du mieux.

Vendredi : aujourd'hui j'ai ressenti beaucoup d'anxiété donc j'ai fait beaucoup de sport. Le truc c'est que le matin j'ai fait une séance jambe (j'ai sué à très grosses gouttes ça faisait longtemps) et le soir j'ai décidé d'aller courir. CHOUETTE IDÉE. L'objectif était clairement de me briser. J'ai croisé tellement de gens ne faisant pas leur jogging en plus... Et j'ai avalé 3 moucherons we love proteins.

Samedi : j’ai finiolé mes candidatures aux M2, après j’ai appelé Fex pendant 2 heures et après j’ai regardé Jojo’s Bizarre Adventure. J’ai évidemment MAL aux jambes donc aujourd’hui j’ai fait les pecs et les épaules. En particulier j’ai fait des pompes et je déteste faire des pompes, mais comme mes séances deviennent un peu routinière (= je vois plus de différence) je pense qu’il faut sortir de sa zone de confort.

Dimanche : ALORS. J’ai des courbatures absolument partout, y’a pas un muscle qui ne me fait pas mal et pourtant j’ai décidé de récurer entièrement ma salle de bain et ma chambre. J’ai fait un whatsapéro avec mes camarades de fac, que malheureusement je ne sais pas si je reverrais vu qu’on candidate aux M2 un peu au pif, donc c’était trop cool de se voir et de critiquer la fac hihihi.

Lundi : L’addition svp !!!

Les gars je préfère pas vous mentir. J’pense qu’on est sur une p’tite dépression des familles (c’est pas que pcq on est confinés rassurez vous). Après, même si c’est dur faut se forcer à voir le positif. Je vais essayer de focus sur les trucs drôles car si j’en fais pas des blagues, je peux pas relativiser. Donc on va dire qu’on sait tous que je passe mes journées à chialer mais au lieu de se demander si ça va on va plutôt parler des trucs rigolo. On peut parler du fait que j’aurais été une youtubeuse beauté archi claquée, on peut parler de vos fruits préférés (noixdecoco) etc. En tout cas moi je pense qu’on peut rire de tout si la blague est bonne. Donc un seul pour cette semaine : l’humour.

#Lundi confinement #quarantined #Confinement #Coronavirus #French side of Tumblr #What the france #Upthebaguette

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you-cancer-vive · 5 years ago

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PROTEIN METABOLISM IN CANCER CACHEXIA

There are metabolic abnormalities seen in individuals with cancer cachexia that arise from malnutrition and malignancy. Protein turnover is evident and high in cancer cachectic patients. Muscle protein synthesis is suppressed during their initial stages of weight loss and is further reduced as their condition progresses. Moreover, protein degradation activation and disrupted oxidative metabolism in skeletal muscles also continue to develop. Thus, protein and amino acid metabolism is clearly affected. These results to the progressive loss of muscle mass, which is the most prominent feature of cancer cachexia (Dodesini et al, 2009). Muscle depletion also reduces chemotherapy effectiveness, increases susceptibility to treatment toxicity, decreases physical function, and impairs psychosocial ability.

The loss of skeletal muscle in cancer patients are due to anorexia and early satiety, reduced muscle protein synthesis, and increased muscle protein breakdown. Inflammation has also negatively contributed to these mechanisms. Inflammatory cytokines such as IL-6 and TNFα contribute to the effects of inflammation on muscle protein metabolism through several pathways.

Impaired muscle protein synthesis

Cancer cachexia disrupts protein translation at several regulatory steps such as initiation, elongation, and termination. The phosphorylation of eIF2α, which impairs translation initiation and overall protein synthesis, is elevated (Hardee, Montalvo, & Carson, 2017). Anabolic and catabolic hormones and energy balance influence signal transduction pathways that regulate protein synthesis via mTOR-related signal transduction pathways. This pathway is the most predominant signaling regulator of translation initiation and are activated by insulin and IGF-1 (Blackwell, 2017). It is also major mediator of anabolic responses in skeletal muscle. Specifically, mTOR activation by insulin or amino acids activates the downstream targets eukaryotic initiation factor binding protein 4E and ribosomal S6 kinase 1, which promote translation initiation, and eukaryotic elongation factor, which stimulates elongation. This pathway is inhibited in cancer cachexia, which corresponds to disrupted S6K1 and 4EBP-1 regulation. A decrease in mTOR activation is also due to AMPK and systemic inflammation. AMPK inhibits mTOR by preventing the interaction with both p70S6K and 4E-BP1 (Durham, Dillon, & Sheffield-Moore, 2009).

Glutamine is the most abundant amino acid in the body. However, glutamine depletion is observed in Cancer Cachexia since glutamine is a regulator of muscle protein synthesis and this is inhibited in the condition. Furthermore, glutamine is a principal fuel for most rapidly proliferating cancers. Tumor cells are major glutamine consumers and they compete with the host for circulating glutamine. Thus, there are changes in glutamine metabolism resulting in glutamine depletion developing with progressive tumor growth (Bode et al, 1996).

Stimulated muscle protein breakdown

There are three main degradation pathways in the skeletal muscle to account for protein degradation. These are ubiquitin-mediated proteasome degradation (UPR), autophagy, and calcium-activated protease calpains.

The over activation of proteolysis is the primary pathway of protein degradation through muscle wasting in Cancer Cachexia (Blackwell, 2017). Muscle protein degradation in cachexia is mainly mediated by the ubiquitin proteasome system which is induced through the activation of E3 ligases, MAFbx, and MurF-1. The FOXO signaling pathway also contributes through the induction of the transcription of these ubiquitin ligases. Thus, the inhibition of FOXO transcription activity prevents muscle fiber atrophy during cachexia (Camargo, 2015). Many of these effects occur through activation of NF-κB by upstream factors such as TNF-α and PIF (Durham, Dillon, & Sheffield-Moore, 2009). During Cachexia, skeletal muscle specifically upregulates muscle specific UPR system, in particular by promoting ubiquitin-ligase MurF1 and Atrogin-1 expression. UPR upregulation is shown by Atrogin-1 messenger RNA and increased protein ubiquitylation. The expression of this ubiquitin ligase is mainly regulated by the transcription factor FoxO3a (FOXO) (Porporato, 2016).

Aside from UPR, the role of autophagy in mediating skeletal muscle wasting is also evident (Porporato, 2016). Autophagy is increased and upregulated in Cancer Cachexia. It is a process of lysosomal degradation where aggregated protein and damaged organelles are engulfed by an autophagosome prior to ultimate joining with lysosome and degradation. These is also contributed by an increase in Reactive Oxygen Species (ROS) production in skeletal muscle (Blackwell, 2017).

Inflammation

Inflammation initiates central anorexic pathways that limit dietary consumption of nutrients. As amino acids are required for muscle protein synthesis, the reduced availability of amino acids in individuals with Cancer Cachexia mainly contributes to their inflammation-induced loss of skeletal muscle mass. Moreover, the reduced supply of amino acids and anorexic response also reduces the exposure to insulin which stimulates muscle protein synthesis. (Durham, Dillon, & Sheffield-Moore, 2009). In relation to insulin resistance, insulin action is not fully able to control catabolic processes in the muscle in Cachectic individuals (Dodesini et al, 2009).

Although liver contributes to cachexia by increasing energy expenditure through gluconeogenesis and reducing VLDL circulation, it worsens inflammation by secreting acute phase proteins and reducing albumin secretion, a process mostly driven by IL-6 and TNFα. This contributes to muscular protein breakdown and adipocytes lipolysis in affected individuals (Porporato, 2016).

Inflammatory-mediated signaling muscle protein synthesis by several mechanisms. TNFα is the most characterized cytokine in cachexia, which promotes anorexia and skeletal muscle wasting mainly through the NF-kB pathway. It activates the transcription factor NF-κB, which inhibits the synthesis of the muscle-specific transcription factor MyoD. TNF-α also influences the anabolic mTOR signaling pathway. It synergizes with interferon gamma and IL-1 in promoting muscle wasting (Porporato, 2016). Inflammatory proteins such as IL-6 also reduce the activation of mTOR directly and indirectly through phosphorylation of AMPK. The infusion of IL-6 increases whole body protein turnover and reduces circulating amino acid concentrations (Durham, Dillon, & Sheffield-Moore, 2009).

References:

Photo retrieved from: https://images.app.goo.gl/kwtG3Tzjmw2Mw6RAA

Blackwell, Thomas Allen, "RNA Sequencing in the Development of Cancer-Cachexia" (2017). Theses and Dissertations. 2434. http://scholarworks.uark.edu/etd/2434

Bode, B. P., Fischer, C., Abcouwer, S., Wasa, M., & Souba, W. W. (1996). Glutamine and Cancer Cachexia. Protein and Amino Acid Metabolism in Cancer Cachexia Medical Intelligence Unit, 139–170. doi: 10.1007/978-3-662-22346-8_11

Dodesini, A. R., Benedini, S., Terruzzi, I., Sereni, L. P., & Luzi, L. (2009). Protein, glucose and lipid metabolism in the cancer cachexia: A preliminary report. Acta Oncologica, 46(1), 118–120. doi: 10.1080/02841860600791491

Durham, W. J., Dillon, E. L., & Sheffield-Moore, M. (2009). Inflammatory burden and amino acid metabolism in cancer cachexia. Current opinion in clinical nutrition and metabolic care, 12(1), 72–77. https://doi.org/10.1097/MCO.0b013e32831cef61

Hardee, J. P., Montalvo, R. N., & Carson, J. A. (2017). Linking Cancer Cachexia-Induced Anabolic Resistance to Skeletal Muscle Oxidative Metabolism. Oxidative Medicine and Cellular Longevity, 2017, 1–14. doi: 10.1155/2017/8018197

Porporato, P. E. (2016). Understanding cachexia as a cancer metabolism syndrome. Oncogenesis, 5(2). doi: 10.1038/oncsis.2016.3

#portfolio

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sensitif01-blog · 7 years ago

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Sejak usia kehamilan 16-22 minggu, sebenarnya ASI sudah terbentuk. Saat plasenta sudah keluar maka dengan sendirinya hormon kehamilan akan menurun, sedangkan hormon menyusui akan meningkat. Saat 1-3 hari setelah melahirkan, ASI cenderung akan bertambah banyak dan semakin sering ASI disedot oleh bayi, maka produksinya akan semakin banyak. Produksi ASI tergantung pada permintaan. Jika Bunda rutin mengosongkan payudara dengan memberikan ASI kepada si kecil ataupun memerahnya, maka produksi ASI bisa lebih berlimpah. Sebaliknya jika payudara tidak sering dikosongkan, maka produksi ASI akan berkurang. Jika payudara yang penuh ASI tidak diperah maka di dalam tubuh Bunda akan terbentuk PIF (Prolacting Inhibiting Factor), yaitu zat yang menghentikan produksi ASI. Asupan nutrisi dari ASI pada bayi dapat membantunya memiliki sistem kekebalan tubuh yang jauh lebih baik, jika dibandingkan dengan bayi yang tidak diberi ASI. Sebab paparan mikroorganisme atau bakteri dalam beberapa bulan pertama usia bayi membantu merangsang sistem kekebalan tubuh. ASI mengandung nutrisi seperti karbohidrat, protein, lemak, vitamin, dan mineral. ASI juga mengandung zat seperti gula dan garam. Bahkan pada ASI, kedua zat tersebut dikandung dalam jumlah yang sudah pas dan seimbang, tak berlebihan. Uniknya, ASI juga merupakan living substance atau cairan hidup. Di dalamnya terdapat sel, hormon, enzim, DNA, dan imuglobin. Semua zat ini membantu meningkatkan imunitas anak dan inilah sebabnya anak yang diberi ASI lebih jarang sakit atau sekalipun sakit lebih cepat sembuh. Tahukah Bunda: “ASI keluar dengan cara diperah dari area yang berwarna hitam (areola), bukan disedot dari putingnya. Jadi apapun bentuk putting Bunda, ASI masih bisa keluar.” #sensitifpedia #fromthismoment #sensitif #pregnancytest #pregnancy #pregnant #momtobe #motherhood #amazingmoment

#amazingmoment #pregnancytest #fromthismoment #pregnant #sensitif #pregnancy #momtobe #motherhood #sensitifpedia

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healthtimetaylor · 5 years ago

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Short chain fatty acids enriched fermentation metabolites of soluble dietary fibre from Musa paradisiaca drives HT29 colon cancer cells to apoptosis.

PMID: PLoS One. 2019 ;14(5):e0216604. Epub 2019 May 16. PMID: 31095579 Abstract Title: Short chain fatty acids enriched fermentation metabolites of soluble dietary fibre from Musa paradisiaca drives HT29 colon cancer cells to apoptosis. Abstract: In this study, the prebiotic potential of soluble dietary fibre extracted from plantain inflorescence (PIF) was investigated. PIF demonstrated prebiotic potential by enhancing the growth of the probiotics under study and thereby hindered colon cancer development. The soluble dietary fibre from Musa paradisiaca inflorescence (PIF) was fermented using Lactobacillus casei and Bifidobacterium bifidum. The fermentation supernatants (LS and BS) were enriched with short chain fatty acids (SCFA) and were able to initiate apoptotic signalling in HT29 colon cancer cells leading to cell death. Both BS and LS exhibited cytotoxic effect; induced DNA damage and enhanced generation of reactive oxygen species in HT29 cells leading to apoptosis. The induction of apoptosis was facilitated by the reduction of membrane potential of mitochondria and ATP synthesis; enhanced delivery of cytochrome c and interference with the expression of pro/antiapoptotic proteins. BS, which exhibited better activity, was further analysed for the identification of differentially regulated proteins by performing two dimensional electrophoresis and MALDI-TOF mass spectrometry. Results emphasized on the fact that, the exposure to BSalteredthe HT29 proteins expression, particularly the upregulation of apoptosis- inducing factor-AIFM1 leading to apoptosis of HT29 cells.

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uicscience · 5 years ago

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A drug to boost cardiac arrest survival

A new four-year, $2.8 million grant from the National Institutes of Health will allow researchers at the University of Illinois at Chicago, together with colleagues from Johns Hopkins University and the University of Texas at Houston, to evaluate the efficacy of two drugs that have the potential to vastly improve survival and cognitive outcomes in people who experience sudden cardiac arrest.

The two drugs, called TAT-PHLPP9c and TAT-PIF, mimic the effects of rapid cooling on the body, which is known to help prevent cardiac damage and mitigate the neurological effects of a heart attack. But cooling the body during and immediately after sudden cardiac arrest is difficult because the vests used to bring down the body’s core temperature are not available in all ambulances or hospitals.

“The best time to cool the body is during CPR, but out in the real world, that is very difficult,” said Dr. Terry Vanden Hoek, professor and head of emergency medicine at the UIC College of Medicine and lead investigator on the grant. “Cooling after the heart has been revived is also beneficial, although cooling during CPR appears to have the most profound benefits.

“Our goal is to deliver these two new biological agents intravenously during CPR so that the patient’s body is ‘cooled’ when it is most beneficial.”

Unlike for other leading causes of death, there are no drugs to treat cardiac arrest, which affects more than 500,000 people annually in the United States. Survival for cardiac arrest outside a hospital is about 7%.

“There are a few things we know help increase survival for out-of-hospital cardiac arrest,” Vanden Hoek said. “One is bystander CPR. Others are emergency responder CPR and cooling the body as soon as possible, preferably starting when CPR starts. But we also need drugs that have the potential to improve survival and long term outcomes and that can be delivered easily on the scene.”

During cardiac arrest, heart cells are unable to contract normally. They also cannot use their normal fuel source — fatty acids — properly. Instead, glucose, a type of sugar, becomes the major fuel source. But using glucose causes cellular stress and leads to increased production of another sugar called sorbitol, which is toxic in large amounts. To dampen the effects of sorbitol, cardiac cells release a compound called taurine, which helps reduce cellular stress. Taurine is very important for both heart and brain health. When taurine leaves the brain, it can lead to cognitive impairment and neurological issues.

In previous work, Vanden Hoek and UIC colleagues identified a small protein that was able to mimic the effects of cooling at the cellular level and is able to quickly permeate cardiac cells to activate an enzyme that supports the metabolism of glucose, preventing damaging cellular stress and toxic sorbitol production. The two new protein drugs are second-generation versions of the original protein, and they target metabolism more precisely and with fewer side effects.

“In mouse studies, our drugs are profoundly protective when it comes to the heart and brain, which take the biggest hits in cardiac arrest,” Vanden Hoek said. In mouse studies, animals given the drugs during cardiac arrest lasting up to 12 minutes were able to be revived and showed no signs of heart or brain damage.

“We are essentially bringing these animals back from the dead with virtually no negative effects,” Vanden Hoek said.

In the new studies, Vanden Hoek and colleagues will test the effects of the two drugs on the heart and brain as well as on cognitive functioning in mouse and pig models of cardiac arrest. They will also use a technique that measures the circumference of the optic nerve as a proxy for brain swelling to see if the drugs can help reduce swelling in the brain during cardiac arrest — a major contributor to negative neurological and neurocognitive outcomes of cardiac arrest. They also will look for biomarkers in the blood that will help them predict outcomes of cardiac arrest and track the effects of their two peptide drugs on outcomes.

Vanden Hoek and colleagues also will explore using their peptides in conjunction with extracorporeal membrane oxygenation, or ECMO. ECMO uses a pump to circulate blood through an artificial lung back into the bloodstream. It is used in some cardiac arrest patients to give the heart a break and a chance to heal.

“We expect to see a synergistic effect in terms of outcomes when using ECMO and our peptides together,” Vanden Hoek said.

Dr. Henry Halperin of Johns Hopkins University is a co-principal investigator and Dr. Henry Wang of the University of Texas at Houston is a co-investigator on the grant.

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stdguide-blog · 6 years ago

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Chlamydia

Chlamydia is a group of infections caused by various types of chlamydia. Affect respiratory, cardiovascular, musculoskeletal, urogenital systems, organs of vision. Urogenital chlamydia is manifestations of inflammatory diseases: urethritis, prostatitis, cystitis, vulvovaginitis, cervicitis, erosion, endometritis and is detected only by specific diagnostic methods. A characteristic symptom is vitreous discharge from the genitourinary tract. Chlamydial infection threat multiple complications, including ascending urinary tract infection, infertility, neurochemicals, joint damage, heart disease and blood vessels, impotence in men.

Urogenital (urogenital) chlamydia is a sexually transmitted infection caused by chlamydia (Chlamydia trachomatis). The problem of urogenital chlamydia is very acute today. In recent years, there has been an increase in chlamydia among sexually active adults (men and women from 20 to 40 years), and among adolescents. Early sexual relations, unprotected sex with casual partners, lack of awareness of possible consequences of such connections put chlamydia on one of the first places in the list of sexual infections. Almost 90 million people are infected with chlamydia every year. Especially susceptible to chlamydia persons with reduced immunity. In 40% of cases chlamydial infection causes various gynecological diseases, in 50% - tubal-peritoneal infertility. Often chlamydia is combined with other sexual infections: gardnerellosis, ureaplasmosis, trichomoniasis, gonorrhea, syphilis, mycoplasmosis, thrush. The combination of several infections exacerbate each other and lengthen the treatment. Women are more susceptible to chlamydia.

The causative agent of urogenital chlamydia-chlamydia trachomatis-is a small bacterium that parasites inside human cells. Chlamydia can exist for a long time in the human body and not manifest itself. When suppressing the protective forces, weakening the body, they begin to actively multiply and cause clinical manifestations of chlamydia. There are 15 different types of chlamydia that cause damage to the eyes, lymph nodes, genitourinary organs, etc.The most common way of transmission of chlamydia is sexual. Infection of the newborn is possible during childbirth, it is accompanied by the development of congenital chlamydia in the child. Much rarer household transmission of chlamydia in the family through bedding and toiletries, linens, etc. Generally from the moment of infection until the first symptoms of chlamydia 1-2 weeks (rarely up to 1 month).

Symptoms of chlamydia

Asymptomatic chlamydia occurs in 67 % of women and 46% of men, which often complicates its diagnosis and treatment, increases the risk of complications. Even with the hidden course of chlamydia, a sick person is potentially dangerous and capable of infecting his sexual partner. Usually the first clinical manifestations of chlamydia infection are observed after 7 to 14 days after sexual exposure.

Men appear mucopurulent or watery discharge from the urethra, itching and burning with the act of urination. There is swelling and redness of the external opening of the urethra. Gradually, the symptoms subside, discharge is observed only in the morning. The acute phase of chlamydia is replaced by chronic with the defeat of the urethra.

In women, chlamydia is manifested by pathological secretions from the vagina of the mucous or mucopurulent character, a yellowish tint, with a smell. Sometimes the discharge is accompanied by itching, burning, low temperature, abdominal pain.

Chlamydia in children often occurs with the defeat of the respiratory system, eyes, ears. If symptoms of chlamydia occur, seek medical advice immediately.

Complications of chlamydia

Urogenital complications of chlamydia in men are chlamydial prostatitis, urethritis, epididymitis.

·�� prostatitis develops when involved in the infectious process of the prostate gland. Chlamydial prostatitis is accompanied by unpleasant sensations and pain in the lower back, rectum, perineum, minor mucous or watery discharge from the urethra, difficulty urinating, violation of potency;

· urethritis occurs with the defeat of the urethra and is characterized by itching in the urethra, frequent painful urge to urinate, mucopurulent discharge. Chronic urethritis caused by chlamydia leads to urethral stricture;

· epididymitis develops with inflammation of the epididymis, which is accompanied by high temperature, swelling and redness of the scrotum, an increase in the epididymis.

Urogenital complications of chlamydia for men is fraught with disruption of spermatogenesis and infertility.

No less dangerous is chlamydia for women, causing various lesions of the female reproductive system. The ascension of chlamydial infection in the genital tract may induce inflammatory changes in the:

· of the cervix – endocervicitis. Chlamydia increases the risk of tumor processes in the cervix;

· the mucous membrane of the uterus – endometritis;

· fallopian (uterine) tubes-salpingitis;

· the appendages of the uterus with salpingo.

Inflammatory processes of the uterus and uterine appendages, followed by the formation of adhesions and scars in the fallopian tubes are the cause of tubal infertility, ectopic pregnancy, spontaneous abortion.

Other consequences of chlamydia in men and women can serve as inflammatory processes of the pharynx, rectum, kidneys, joints, lungs, bronchi, etc.one of the serious complications of chlamydia is Reiter's disease, characterized by a triad of clinical manifestations: conjunctivitis, urethritis, arthritis. Repeated infection with chlamydia significantly increases the risk of complications.

A special danger is the chlamydia of newborns that occurs as a result of infection of the child from a sick mother during childbirth. The main forms of congenital chlamydia are:

· chlamydial conjunctivitis (ophthalmoplegia) - inflammation of the mucous membrane of the eye

· generalized form of chlamydia-damage to the heart, lungs, liver, digestive tract

· encephalopathy accompanied by seizures and respiratory arrest

· chlamydial pneumonia is an extremely severe form of pneumonia with a high mortality rate.

Diagnosis of chlamydia

TrachomatisДиагностику Chlamydia of chlamydia in men often spend urologists. A visit to the venereologist is necessary to exclude other STIs that the patient could have contracted along with chlamydia. Women need advice from a gynecologist.

The General cytological smear of the separated urethra, vagina and cervix does not give an objective picture of the presence of chlamydia. The number of white blood cells in this case may be slightly increased or be within normal limits. With the advent of PCR diagnosis (polymerase chain reaction), venereology has received the most accurate way to detect chlamydia, allowing to detect in the test material, even a small amount of the pathogen. The accuracy of the result at PCR reaches 95%.

Informative with an accuracy of 70% methods of ELISA (enzyme immunoassay), revealing the presence of antibodies to the pathogen and PIF (direct immunofluorescence) – microscopy of smears, painted in a certain way.

For the diagnosis of chlamydia is also used bakposev taken material and determination of sensitivity to antibiotics.

As a material for the diagnosis of chlamydia use urine, blood, sperm in men, discharge from the genitals, scraping cells of the affected organ.

Treatment of chlamydia

As with the treatment of any bacterial infection, chlamydia uses antibacterial drugs. Since the causative agent of chlamydia chlamydia trachomatis is a parasitic intracellular microorganism, the choice of antibiotics is limited to those drugs that penetrate into the cells. Such drugs include antibiotics macrolides, tetracyclines and fluoroquinolones. When selecting antibiotics, the presence of mixed infection (Mycoplasma, Gardnerella, Ureaplasma) for their simultaneous treatment is taken into account.

In addition to the antibiotic, the treatment regimen of chlamydia include immunomodulators (interferon, meglumin acridonacetate), antifungal drugs (nystatin, fluconazole), multivitamins, enzymes (Pancreatin), bacteriophages (staphylococcal, protein, etc.), probiotics, physiotherapy (ultrasound therapy, magnetotherapy, ionophoresis and electrophoresis with drugs).

For local treatment of chlamydia, vaginal and rectal candles, baths, tampons, enemas are used.

During the course of treatment (an average of 3 weeks) it is recommended to exclude sexual contact, alcohol, spices, spicy food, excessive physical activity.

Treatment of chlamydial infection is a complex medical problem, and it should be solved taking into account the individuality of each patient. In the treatment of chlamydia can not recommend the use of ready-made algorithms. In elderly people with comorbidities, should take into account the state of immunity, intestinal microflora and urogenital tract.

Prevention of chlamydia

Chlamydia is an infection that is easier to avoid than to get rid of it. The main rules of prevention of chlamydia, as well as other sexual infections, are:

· having a permanent sexual partner;

· avoiding casual sex or using condoms;

· examination for infection, if there was an accidental unprotected sexual intercourse;

· notification of all sexual partners in case of confirmation of the diagnosis of chlamydia;

· examination of women planning pregnancy for hidden infections (including chlamydia) and careful management of pregnancy to prevent the disease in the newborn;

· abstinence from sexual activity during the treatment of chlamydia.

Prognosis of chlamydia

When detecting chlamydia in one of the sexual partners, it is very important to examine and treat the other for the presence of infection, even in the absence of obvious symptoms of the disease. If one of the sex partners infected with chlamydia does not undergo treatment, the other, treated, can be infected again.

To control the cure, diagnosis by ELISA and PCR methods is used 1.5-2 months after the completion of the course of therapy (in women – before menstruation). The criteria for cure-negative results of tests for chlamydia and the absence of symptoms of chlamydia.

Acute uncomplicated chlamydia with simultaneous treatment of all sexual partners gives a favorable prognosis for a complete recovery. If chlamydia is started (late diagnosed, short-lived, complicated), then in the long term can develop various disorders of sexual function – from impotence to infertility.

Sousres:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3818592/

https://std-symptoms.com/chlamydia

https://www.womenshealth.gov/a-z-topics/chlamydia

#std #symptoms #health #medicine

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fruitybargonodactylussmithi-blog · 7 years ago

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yeast-papers · 8 years ago

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Protein-Protein Interactions of the Baculovirus Per Os Infectivity Factors in the PIF Complex.

Pubmed: http://dlvr.it/NG4MJp

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internationalnewslive · 8 years ago

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Easy Quinoa Recipes to Make 2017 Healthy

pIf you are looking to compensate for all the unhealthy eating you’ve indulged in; and are not prepared to compromise on taste, then quinoa, a gluten-free protein-rich seed, is your saviour./p pEasy and nutritious, here is a list of quinoa recipes to help you keep your New… http://internationalnewslive.com/easy-quinoa-recipes-to-make-2017-healthy/

from WordPress https://internationalnewsliveblog.wordpress.com/2017/01/09/easy-quinoa-recipes-to-make-2017-healthy/

#Uncategorized #International Live News

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intlnewslive · 8 years ago

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Easy Quinoa Recipes to Make 2017 Healthy

pIf you are looking to compensate for all the unhealthy eating you've indulged in; and are not prepared to compromise on taste, then quinoa, a gluten-free protein-rich seed, is your saviour./p pEasy and nutritious, here is a list of quinoa recipes to help you keep your New... from International Live News http://internationalnewslive.com/easy-quinoa-recipes-to-make-2017-healthy/

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marykramer1 · 8 years ago

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Easy Quinoa Recipes to Make 2017 Healthy

pIf you are looking to compensate for all the unhealthy eating you’ve indulged in; and are not prepared to compromise on taste, then quinoa, a gluten-free protein-rich seed, is your saviour./p pEasy and nutritious, here is a list of quinoa recipes to help you keep your New… from International Live News http://internationalnewslive.com/easy-quinoa-recipes-to-make-2017-healthy/

from International News Live http://internationalnewslive1.tumblr.com/post/155615919089

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you-cancer-vive · 5 years ago

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GENE EXPRESSION

DNA is the genetic material of all organisms. This DNA material is divided up into functional unit called genes, and each gene provides instructions for the cell’s function. The central dogma describes transcription and translation, wherein the information in genes flows into proteins. In transcription, and RNA copy of the DNA segment is synthesized, whereas in translation, RNA is translated into protein.

Cancer results from a gene that is not normally expressed in a cell but may be expressed at high levels due to mutations or alterations in gene regulation. Alterations in histone acetylation, increased translational control, and protein modification are observed in cancer cells. Cancer can be described as a disease of altered gene expression since there are many proteins that are activated which affect the overall activity of the cell. This disease can also be detected by changes in epigenetic regulation, transcription, RNA stability, protein translation, and post-translational control. However, these changes do not occur all at once (Lumen, 2020).

Cancer Cachexia develops a wide range of dysfunctions from insulin and IGF-1 resistance to induction of mitochondrial uncoupling proteins and fat tissue browning which results to uncontrollable increased energy expenditure and heat generation. Tumor cells also actively promote tissue wasting by secreting specific factors such as microRNAs (Porporato, 2016). Moreover, AMPK activity is disrupted during cancer cachexia progression. Thus, it can contribute to altering skeletal muscle metabolism and gene expression. There is chronically elevated muscle AMPK activity during cachexia, which coincides with the suppression of mTORC1 signaling and disrupted mitochondrial quality control mechanisms. While AMPK activation by systemic IL-6 also corresponds with mTORC1 suppression, AMPK inhibition rescues IL-6-induced suppression of mTORC1 signaling in C2C12 myotubes (Hardee, Montalvo, & Carson, 2017).

miRNAs also play a major role in the regulation of the transcription of several genes involved with skeletal muscles. miRNA-486 decreases FoxO1 protein expression and promotes FoxO1 phosphorylation to suppress E3 ubiquitin ligases (Camargo, 2015). Moreover, skeletal muscle protein synthesis in cachexia reduces when dsRNA-dependent protein kinase (PKR) is activated by the tumor-secreted proteolysis-inducing factor (PIF), which is a potential inhibitor. This happens because of phosphorylation of eukaryotic initiation factor (eIF) 2, which interferes with the activity of eIF2B to promote translation initiation (Durham, Dillon, &. Sheffield-Moore, 2009). The inhibition of protein synthesis in muscle also reduces both RNA content or its protein synthesizing capacity and RNA activity such as the amount of protein synthesized by RNA. Levels of myosin follows the decrease in total protein, while actin levels remained constant (Bhogal, Lorite, & Tisdale, 2006).

References:

Photo retrieved from: https://images.app.goo.gl/hcZ1UXPxYPAnC17a7

Bhogal, Lorite, M., & Tisdale, M. (2006). Changes in Nucleic Acid and Protein Levels in Atrophying Skeletal Muscle in Cancer Cachexia. ANTICANCER RESEARCH, 26(6), 4149–4154. Retrieved from http://ar.iiarjournals.org/content/26/6B/4149.long

Camargo, R. (2015). Cancer Cachexia and MicroRNAs. Inflammation in Cachexia. doi: https://doi.org/10.1155/2015/367561

Cancer and Gene Regulation. 2020. Lumen Candela. Retrieved from https://courses.lumenlearning.com/boundless-biology/chapter/cancer-and-gene-regulation/

Porporato, P. E. (2016). Understanding cachexia as a cancer metabolism syndrome. Oncogenesis, 5(2). doi: 10.1038/oncsis.2016.3

#portfolio

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