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Quality of Life of Child Labor with a Focus on Developing World: A Sociological Appraisal
Quality of Life of Child Labor with a Focus on Developing World: A Sociological Appraisal in Biomedical Journal of Scientific & Technical Research
Child labor creates problems within children now, and for the years to come. Many of the children will face disorders as far as their quality of life is concerned. Many of them would not be able to get sufficient food, adequate schooling, etc. So, the upcoming generations of child labor may also repeat the same cycle in the developing world. The child laborers of the present era are equipped with the cell phones allowing them to travel more and settle down in desired lands alone or with their families. Child laborers easily marry in young ages, and consequently get many children. They easily access to narcotics and commit crimes. Having low quality of life, they transfer it to the next generation as well. Therefore, child labor needs care, supervision and reforms. Supervision on present young families, and use of family planning programs will control the child labor in future. That is what the Third World countries must pay attention to, in order to build healthy generations. In recent years International Labor Organization, Unicef and other UN Departments have intervened to eliminate the present social disorder.
For more articles in Journals on Biomedical Sciences click here bjstr
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#journals on medical microbiology#journals on medical informatics#journals on biomedical engineering#biomedical open access journals#medical and medicinal journal
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I wish "your favorite sidekick" was a book instead of a fanfic so I could use "Excellently written,
Nearly medically accurate!" - actual medical doctor
As one of those quotes on the back.
#adventures of a fic writer#given my complete lack of any medical training whatsoever past a community college microbiology class#i think this speaks to the power of... well of being able to read medical journals without vomiting tbh
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Lavender
Lavandula officinalis
Known as: Elf leaf, nard, nardus & spike
Related plants: A member of the mint family Lamiaceae, there are genus of 47 known species of lavender. It includes well known plants such basil, mint, rosemary, sage, savory, marjoram, oregano, hyssop, thyme, lavender, and perilla, as well as catnip, salvia, bee balm, wild dagga & oriental motherwort.
Parts used: Flowers
Habitat and cultivation: This flowering plant is native to the the Mediterranean
Plant type: Perennial
Region: Most are hardy from Zones 5 to 9 | Spanish Lavender (L. stoechas) is only hardy in Zones 7 to 9.
Harvest: You can harvest all the budding spikes or flowers on your plant during the growing season but avoid cutting into woody growth. Don't want to take more than 1/3 of the plant at this time & limiting your harvest to flowers and buds should keep you within recommended limits. As first frost approaches, snip off woody, leafy stems & branching. You can safely take up to 2/3 of the plant at this time. Harvesting too early can stimulate more growth which you don't want since the lavender is moving into winter dormancy.
Growing tips: To grow lavender successfully it needs well-drained soil, full sun & may be a good idea to check the PH beforehand because soil too acidic may kill off your plants. It survives well in dry conditions, so you'll only have to water when the top 2 inches of soil are dry. Plant lavender in spring, once all chances of frost have passed. This beautiful, fragrant herb is a great addition to raised beds, in-ground gardens, and growing in containers spacing plants 12 to 18 inches apart.
Medicinal information: Taking lavender products by mouth, including teas and a specific oil supplement or inhaling lavender oil as aromatherapy, seem to reduce symptoms of depression & anxiety. Lavender oil is believed to have antiseptic and anti-inflammatory properties, which can help to heal & burns & bug bites. Some studies suggest that consuming lavender as a tea can help digestive issues such as vomiting, nausea, intestinal gas, upset stomach, & abdominal swelling. A study published in the Journal of Medical Microbiology found that lavender oil could be effective in combating antifungal-resistant infections. Using it as aromatherapy can also reduce colic symptoms & menstrual cramp pain.
Cautions: Lavender essential oil is possibly safe when inhaled as aromatherapy, but applying products that contain lavender oil to the skin is possibly unsafe for young cis males who haven't reached puberty. The oil seems to have hormone-like effects that could disrupt normal hormones & in some cases, this has resulted in breast growth.
Lavender might cause sleepiness and slowed breathing. Taking lavender with sedative medications might cause breathing problems and/or too much sleepiness.
Lavender might slow down the central nervous system. If used with anesthesia and other medications given during and after surgery, it might slow down the central nervous system too much. Stop using lavender at least 2 weeks before a scheduled surgery.
Magickal properties
Gender: Masculine
Planet: Mercury
Element: Air
Deities: Aradia, Elves, Faeries, Hecate & Saturn
Magickal uses:
• Place in sleep pillows to encourage peaceful sleep
• Wear as a perfume to attract a new love
• Rub on paper when writing love spells or notes for added power
• Add with rosemary to a satchet for preserve chastity
• Scatter around your home to invite protection & purifying energies
• Use in a ritual bath to lighten feelings of depression or sadness
• Wear or use in an amulet to discourage cruelty from a spouse
• Drink lavender tea before bed to aid in astral travel or dream magick
• Burn as an incense for meditation or spirit work
• Use in spells to strengthen friendships
• Purify your ritual candles & tools with a drop of oil to release any negative energies contained within them
• Hang above your door protect against evil spirits , for home blessings & to cleanse all who enter
• Rub the oil on to the base of the skull or temples to help cure the nervous exhaustion that sometimes happens after intensive magickal workings
#herb of the week#magical herbs#herbalism#lavender#witchblr#wiccablr#paganblr#witch community#witches of tumblr#witch tumblr#witchcraft#spells#spellwork#grimoire#book of shadows#spellbook#tumblr witch#witch tips#beginner witch#baby witch#beginner witch tips#witchcore#correspondence#green witchery#GreenWitchcrafts#green witchcraft#traditional witchcraft#witch#witch guide#green witch
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Old news (Published March, 2023)
Also preserved in our archive
Something that needs to be remembered when your CDC and medical professionals are claiming that "an infection is just as good as a booster" in regards to covid. It literally isn't.
NIH-funded study suggests need to boost CD8+ T cell response after infection.
What The magnitude and quality of a key immune cell’s response to vaccination with two doses of the Pfizer-BioNTech COVID-19 vaccine were considerably lower in people with prior SARS-CoV-2 infection compared to people without prior infection, a study has found. In addition, the level of this key immune cell that targets the SARS-CoV-2 spike protein was substantially lower in unvaccinated people with COVID-19 than in vaccinated people who had never been infected. Importantly, people who recover from SARS-CoV-2 infection and then get vaccinated are more protected than people who are unvaccinated. These findings, which suggest that the virus damages an important immune-cell response, were published today in the journal Immunity.
The study was co-funded by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, and led by Mark M. Davis, Ph.D. Dr. Davis is the director of the Stanford Institute for Immunity, Transplantation and Infection and a professor of microbiology and immunology at Stanford University School of Medicine in Palo Alto, California. He is also a Howard Hughes Medical Institute Investigator.
Dr. Davis and colleagues designed a very sensitive tool to analyze how immune cells called CD4+ T cells and CD8+ T cells respond to SARS-CoV-2 infection and vaccination. These cells coordinate the immune system’s response to the virus and kill other cells that have been infected, helping prevent COVID-19. The tool was designed to identify T cells that target any of dozens of specific regions on the virus’s spike protein as well as some other viral regions. The Pfizer-BioNTech vaccine uses parts of the SARS-CoV-2 spike protein to elicit an immune response without causing infection.
The investigators studied CD4+ and CD8+ T-cell responses in blood samples from three groups of volunteers. One group had never been infected with SARS-CoV-2 and received two doses of the Pfizer-BioNTech COVID-19 vaccine. The second group had previously been infected with SARS-CoV-2 and received two doses of the vaccine. The third group had COVID-19 and was unvaccinated.
The researchers found that vaccination of people who had never been infected with SARS-CoV-2 induced robust CD4+ and CD8+ T-cell responses to the virus’ spike protein. In addition, these T cells produced multiple types of cell-signaling molecules called cytokines, which recruit other immune cells—including antibody-producing B cells—to fight pathogens. However, people who had been infected with SARS-CoV-2 prior to vaccination produced spike-specific CD8+ T cells at considerably lower levels—and with less functionality—than vaccinated people who had never been infected. Moreover, the researchers observed substantially lower levels of spike-specific CD8+ T cells in unvaccinated people with COVID-19 than in vaccinated people who had never been infected.
Taken together, the investigators write, these findings suggest that SARS-CoV-2 infection damages the CD8+ T cell response, an effect akin to that observed in earlier studies showing long-term damage to the immune system after infection with viruses such as hepatitis C or HIV. The new findings highlight the need to develop vaccination strategies to specifically boost antiviral CD8+ T cell responses in people previously infected with SARS-CoV-2, the researchers conclude.
Article F Gao, et al. Robust T cell responses to the Pfizer/BioNTech vaccine compared to infection and evidence of attenuated CD8+ T cell responses due to COVID-19. Immunity DOI: 10.1016/j.immuni.2023.03.005(link is external). (2023). www.cell.com/immunity/fulltext/S1074-7613(23)00125-5
#mask up#covid#pandemic#wear a mask#public health#covid 19#wear a respirator#still coviding#coronavirus#sars cov 2#covid pandemic#covid conscious#covid is airborne#covid isn't over#covid19#covidー19#covid is not over#covid is still a thing#covid is not the flu
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Complement system
1. Activation: The complement system can be activated through three main pathways: the classical pathway, the alternative pathway, and the lectin pathway. Each pathway involves different initiating events but converges on a common cascade of reactions.
2. Cascade of Reactions: Once activated, the complement system triggers a cascade of enzymatic reactions that result in the cleavage of complement proteins. This cascade ultimately leads to the formation of several key components, including C3b, C4b, and C5b.
3. Opsonization: C3b and C4b are opsonins, which means they can bind to pathogens and label them for phagocytosis by immune cells like macrophages and neutrophils. This enhances the removal of pathogens from the body.
4. Inflammation: Complement activation also results in the release of small peptides called anaphylatoxins, such as C3a and C5a. These peptides promote inflammation by increasing blood vessel permeability and attracting immune cells to the site of infection.
5. Membrane Attack Complex (MAC): The final step of complement activation involves the assembly of the membrane attack complex (MAC). C5b, C6, C7, C8, and multiple C9 molecules come together to form the MAC, which can create pores in the membranes of target cells, leading to cell lysis and destruction of pathogens.
References:
1. Walport, M. J. (2001). Complement. First of two parts. New England Journal of Medicine, 344(14), 1058-1066.
2. Ricklin, D., Hajishengallis, G., Yang, K., & Lambris, J. D. (2010). Complement: a key system for immune surveillance and homeostasis. Nature Immunology, 11(9), 785-797.
3. Merle, N. S., Church, S. E., Fremeaux-Bacchi, V., & Roumenina, L. T. (2015). Complement system part I – molecular mechanisms of activation and regulation. Frontiers in Immunology, 6, 262.
Please note that for the most current and detailed medical information on the complement system, I recommend consulting recent textbooks or academic journals in immunology and microbiology.
#science#biology#college#education#school#student#medicine#doctors#health#healthcare#immunology#immune system#complement system
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In a rare case, a black bear in Connecticut has tested positive for rabies, sparking a warning from state wildlife officials.
The bear was a wild female adult discovered in Canton, Connecticut, in February 2023. Like other bears, it should have been hibernating during the winter months. However, due to mobility issues on the left side of its body, the bear was seen falling over, lying down, and not responding to human presence, according to a new paper in the journal Microbiology Resource Announcements.
The bear was observed for 24 hours before being euthanized by a Connecticut conservation officer. Its body was taken to the Connecticut Veterinary Medical Diagnostic Laboratory (CVMDL) at the Unversity of Connecticut's College of Agriculture, Health and Natural Resources for a post-mortem.
After the CVMDL sequenced the bear's brain tissue during the necropsy, they discovered that it was infected with rabies. This was only the second bear the lab had encountered with the virus.
The Connecticut Department of Energy and Environmental Protection (DEEP) has advised the public to avoid any animal that "appears to be distressed, which may include symptoms like stumbling, staggering, walking in circles, dragging a limb or the hind end, or otherwise acting strangely," according to a statement from the University of Connecticut.
Rabies is a viral disease that affects the central nervous system of mammals, causing the inflammation of the brain. The virus is typically transmitted through the saliva of infected animals via bites, scratches, or even mucous membranes and open wounds. It is almost always fatal once symptoms appear, which generally manifest after around 2–3 months and can initially include fever, headache and weakness, progressing to agitation, anxiety, hallucinations, a fear of water, excessive salivation, and lack of coordination.
If an animal displays neurological symptoms, such as stumbling and falling over, then scientists will first test for rabies. If the test comes back positive, CVMDL does not proceed with a full necropsy to protect staff.
"We rule out rabies because we don't want to do a necropsy that could expose people unnecessarily," Guillermo Risatti, CVMDL director and professor at the University of Connecticut, said in the statement. "So, once we detect rabies, that's it. We don't do anything else with the carcass."
The CVMDL scientists sequenced the entire genome of the rabies virus found inside the bear to compare it with a gene bank of other sequences from animals infected with rabies across the world. They found that the virus in the bear—which was the only bear sample on the whole database—most closely resembled a virus sequence from a raccoon in New England.
By comparing these strains of rabies, scientists can investigate how the virus spreads between animals in certain areas.
"That's the value—to see what the virus looks like and be able to distinguish a new virus coming into the area," Risatti said. "All of the sequencing is done by us, here in house. So that is the value. We have created a sequencing lab inside a diagnostic lab that is allowing us to dig more into what is going on."
Only 1 to 3 cases are reported in humans in the United States annually. If a human contracts rabies, they need to receive post-exposure prophylaxis as soon as possible, which can be up to 100 percent effective at preventing the disease. Around 60,000 people receive this post-exposure prophylaxis in the U.S. every year.
Humans most at risk are those living in areas where wildlife that commonly contract rabies, including bats, raccoons, skunks, and foxes, are common. While this case of rabies in a bear is rare, it may become more common in the future, as sightings of black bears in Connecticut have increased lately.
Nine bears were submitted to the CVMDL for testing in 2023 alone, compared to seven between 2019 and 2022.
The DEEP advises calling the local animal control officer or police department if you spot a potentially rabid animal, staying well clear of it, and definitely not attempting to pick it up.
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Leishmaniasis
Case Reports, like we're on a episode of house
23M in Kenya, presenting with months of LOW, persistent fevers, and abdo fullness, found to have massive splenomegaly.
examination: massive splenomegaly (10 cm below costophrenic margin, and will definitely cross midline) and hepatomegaly
pancytopaenic on bloods, plt's down to 40s
diagnosis confirmed on BMAT (parasite seen)
normal HIV, liver and kidney function
Bodies seen on the BMAT below are part of the lifecycle of the parasite that is intracellular, hence you can see the macrophages/neutrophils loaded with them, even bursting
What is it:
think of it when you get a patient with pancytopaenia and hepatosplenomegaly, who either traveled to or is in/from a tropical/subtropic region (where sand flies are)
cause - protozoa parasite Leishmania, transmitted by infected sandflies
Epidemio (when to consider it)
tropics, subtropics (South America, Asia, AFrica), Southern Europe
Microbiology/Transmission
parasite, replicates intracellularly (Leishmania donovani)
transmitted in sand flies (can be unnoticeable and usually bite in dawn or dusk - evenings or night), can also be transmitted via needles/blood
more common in rural areas
I've simplified this, but is more extensively covered in StatPearls and Wiki (there's different species of Leish and sandflies that transmit it)
once bitten, the protozoa are phagocystosed by skin macrophages, which then becomes full of the "bodies" (part of the lifecycle). Eventually these burst to release more of the bodies that infect more macrophages
they eventually are spread via blood to liver/spleen/BM and LNs
Random history:
ancient, records of disease date back to Egyptian mummies from 3000 BC --> positive DNA amplication for Leishmania and on papyrus from 1500 BC
multiple physicians from different times have described the disease, but it's named for 2 who described the parasite's intracellular ovoid body stage in smears from infected patients in India: Lt General William Boog Leishman and Captain Charles Donovan (Ronald Ross named the bodies after the 2 --> "Leishman Donovan bodies"
significant disease in Allied troops in Sicily in WWII, called "jericho buttons" (image on wiki from a WWI trooper serving in the middle east)
Leishman: Scottish pathologist and British Army medical officer, later it's director general in the 20s, did extensive research into the parasite named for him by Sir Ronald Ross. He mistook the parasite he observed for trypanosomes (cause of Chagas in South America and African sleeping sickness in Africa)
Donovan: Irish parasitologist, medical officer in India, observed an epidemic across India just after the rebellion of 1857, discovered the "bodies" in spleen tissue as the causative agent for what the locals called "kala azar" (severe visceral leishmaniasis - see below)
Donovan also discovered the "bodies" of Klebsiella granulomatis, hence these too are named after him (cause of ulcerative granulomas)
It became scandalous as both wanted credit for the "discovery" of this newly identified organism. So Sir Ronald Ross named it for both of them.
Sir Ron, by the way, won a Nobel in Medicine for discovering that malaria is transmitted via mossies (this was also a source of scandal, he was meant to share it with another physician who he accused of fraud - and they never received the award)
finally, it was actually a Russian physician who identified it first, but well, he published in a little known Russian journal which was promptly forgotten.
Clinical features
cutaneous type vs visceral organ type (spleen, liver, bones)
From wiki
can be asymptomatic
cutnaeous: can be there for years and resemble leprosy, causes an open chronic wound (most common), incubation 2-4 weeks on average (nodules at site of inoculation that eventually form ulcers), can heal spontaneously in 2-5 yrs
in diffuse cutaneous cases, can affect face, ears, extensor surfaces
can be muscosal = eg nasal symptoms/epistaxis, severe: perforated septum, this occurs in 1/3 after resolution of cutaenous symptoms (can be severe/lifte threatning, as it can affect vocal cords and cartilage, but oddly not bone)
visceral (incubation periods of up to years until immuncompromise): fever, weight loss, hepatosplenomegaly (spleen more than liver), pancytoaepnia, high total protein and low albumin with hypergammaglobulinaemia
this has seasonal peaks related to sandfly habits and humidity
interestingly it is an infective cause of massive splenomegaly, such that it crosses the midline
Extreme - but noticeable hepatosplenomgealy/abdo fullness, from medscape
can be atypical in HIV co infected patients, LAD in seom regions like Africa
Kala azar = black fever in some severe cases (fatal due to secondary mycobacterial infection or bleeding), refers to damage fto spleen, liver and anaemia
invstigations:
serology not great (minimal humoral response to the parasite), so often requires histopath (tissue sample) for which BMAT is safest in visceral organ involvement
visualisation of amastigotes (or Leishman-Donovan bodies), as intracellular --> can be seen in macrophages (small round bodies) post Giemsa staining
PCR of DNA also possible (as done in the Egyptian mummies)
Image source:
Treatment
liposomal amphotericin B (holy shit strong stuff) in visceral, PO: miltefosine (caution in pregnancy), all have significant ADRs, or paromycin. however, mortality of 10% if visceral left untreated
mixed results with azoles
in HIV co infection - start the HAARTs! can improve survival, mortality is 30% in HIV patients
cutaneous: stibolgluconate (have never heard of these drugs) and megluaine antimoniate, but limited disease often spotnaeously gets cleared by the innate system
prevention:
use DEET insect repellant at dawn and dusk
loose fitting clothing that covers all skin
no vaccine (were attempts at vaccinating dogs, which decreased rates)
sandflies are smaller than mossies, so requires small netting
Differentials for hepatosplenomegaly
Sources:
WHO guidelines
CDC guidlelines
Wiki - Haven't covered pathophysio, but wiki does extensively
StatPearls
DermNet - great resource for all things derm, that my derm colleagues pointed out to me
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Emerging infectious agents: an unusual case of Metapneumovirus pneumonia in an adult patient by Graziana Francesca Greco in Journal of Clinical Case Reports Medical Images and Health Sciences
Abstract
Human Metapneumovirus (hMPV), a relatively new virus, is a common cause of acute respiratory infection, especially common in the pediatric population. Despite hMPV infection in adults is possible, this rarely results in serious clinical manifestation. Here, we describe a hypoxemic respiratory failure related to pneumonia in an adult patient in whom hMPV was detected in respiratory samples.
Keywords
Human Metapneumovirus; SARS-CoV-2; Covid-19.
CASE HISTORY
A 61-yr-old caucasian man presented to the Emergency Department (ASST Mantua Hospital, Mantua, Italy) with fever up to 39°C, poorly responsive to antipyretics, nocturnal dyspnea and productive cough with mucus-purulent sputum for three days. On physical examination he appeared in good general condition, collaborating and oriented. The following parameters were recorded: blood pressure 140/90mmHg, heart rate of 100 beats min-1; respiratory rate of 23 breaths min-1; and body temperature of 38.4°C. His arterial oxygen saturation on room air was 87%. Chest examination revealed abnormal breath sounds with rhonchi and fine crackles in the middle lobe and inferior lobes bilaterally, no wheezes were heard. Laboratory findings revealed lymphocytosis (81000 x 103/µl), low platelet count (113000 x 106/µl) and an increase in alanine transaminase value (59 U/L), total bilirubin value (1.13 mg/dL) and CPR value (112 mg/L). Room air arterial blood gas analysis showed a normocapnic hypoxemia: pH 7.43, carbon dioxide tension 40.5 mmHg, oxygen tension 60.4 mmHg, and HCO3 24 mmol L-1. The SARS-CoV-2 antigen detection test on nasopharyngeal swab was negative. A chest radiograph showed multiple, small, patchy opacities in the right upper and middle lobe and no pleural effusion was observed. Based on these findings he was admitted to the Respiratory Department.
His medical history included chronic lymphocytic leukemia in follow-up which did not require any specific treatment. He denied taking any medications or to be a smoker, he drinks a glass of wine once a day and has no known allergies. The patient was a farmer who cultivates wheat and maize but he had no animal exposure and no travel history in the last few years. There is no family history or childhood history of respiratory complaints. He was vaccinated with three dosesagainst the SARS-CoV-2 infection (Pfizer) but not against the influenza virus.
Based on the patient’s presentation and testing results, on suspicion of bacterial pneumonia he was empirically treated with IV Piperacillin/Tazobactam, the patient required oxygen support at 3L min-1 and an inhalation therapy with Beclomethasone/Formoterol was set up ex adiuvantibus. In the following days, several microbiological investigations were carried out to determine the etiology of pneumonia: blood culture, urinoculture, sputum culture, Legionella, Haemofilus and Pneumococcus serologic tests, Legionella pneumophila and Pneumococcal urinary antigen test, all of which were negative.
A nasopharyngeal swab FilmArray Respiratory Panel Assay (NP FARP) was then requested: it was positive for human Metapneumovirus and the result was confirmed by repeating the test. For non responder fever and further increase of CPR (230 mg/l) and PCT (0.27 ng/ml), Levofloxacin and later Meropenem were added in the perspective of a resistant bacterial etiology. On the 6th hospitalization day a chest computed tomography (CT) scan was obtained (Figures 1 and 2) which demonstrated large opacities with gradient borders, distributed in the peribronchial area at the right upper lobe, middle lobe and both the lower lobes; they tended to the confluence configuring parenchymal consolidations with aerial bronchogram at the level of the cost-phrenic angle. Imaging also showed bilateral hilar and mediastinal lymphadenopathy (max diameter 3.4 x 2 cm), splenomegaly and absence of pleural effusion. Blood chemistry tests for HIV, Aspergillus antigen and galactomannan were also investigated but turned out negative. To rule out other infectious agents the patient underwent bronchoscopy with bronchoalveolar lavage (BAL) into the middle lobe. BAL provides material for various microbiological and cytological tests: Gram stain, culture, Koch’s bacillus DNA, Galactomannan, Cytomegalovirus and P. Jirovecii and immunological analysis were negative. From respiratory virus panel on BAL only human Metapneumovirus was isolated, this unique microbiological data was according to the NP FARP’s result, thus supporting and confirming the new hypothesis of a viral pneumonia in an adult patient with probable secondary mild immunosuppression due to his hematological disease. About ten days after entering the ward, there was a gradual decrease of CPR and a progressive improvement in clinical conditions and respiratory function to allow the suspension of oxygen therapy. At the end of hospitalization, pulmonary function tests were performed and showed a restrictive syndrome (FEV1/FVC 76.2, TLC 68% and VC 79% of predicted) and mild reduction of diffusion capacity (DLCO 62% and KCO 99%), probably representing the residual functional impairment due to viral pneumonia. The patient finally suspended all therapies and at discharge was referred for a one-month follow-up visit.
DISCUSSION
Human Metapneumovirus (hMPV), a relatively new virus first discovered in 2001, has been detected in 4-16% of patients with acute respiratory infections [1] [2] [3]. In particular, a recent review of 48 previous articles, including 100,151 patients under the age of five hospitalized for CAP, identified this virus as a cause of pneumonia in 3.9% of patients [4]. A recent study of 1386 hospitalized adult patients identified hMPV pneumonia in only 1.64%, indicating that it was much less common than in the infant population [5]. Metapneumovirus causes disease primarily in infants, but rarely can infect immunosuppressed individuals and elderly as well. Seroprevalence studies have shown that 90-100% of 5-10 years old children have previous infection [6]. Reinfection can occur during adulthood because of defected immunity acquired during the first contact with hMPV and/or because of different viral genotypes. The incubation period varies widely but is typically 3-5 days. The disease severity depends on the patient's condition and it ranges from mild upper airway infection to life-threatening pneumonia or bronchiolitis [7]. Clinically, Metapneumovirus infection is often indistinguishable from RSV infection, particularly in the pediatric population, and common symptoms include hypoxemia, cough, fever, upper and lower airway infections and wheezing [8]. hMPV infant patients are often hospitalized for bronchiolitis and pneumonia [9]. In young adults, a flu-like syndrome with fever may occur in a small number of instances, but infection in geriatric subjects may cause severe clinical manifestations such as pneumonia and, in rare cases, death [10].
As described in this case, it was not surprising that antibiotics and corticosteroids were administered in most patients infected with Metapneumovirus mainly for two reasons: in most cases the specific diagnostic tests for hMPV are not carried out at admission and/or physicians prefer to continue steroid and antibiotic treatment to control potential unidentified bacterial infections in patients in which no etiological agent had been identified associated with hMPV infection. The overuse of these drugs could therefore be reduced through the adoption at admission of specific diagnostic tests for such etiological agent, especially if specific risk factors are present (age, immunodepression, etc.). In addition, the adoption of such tests could reduce the nosocomial spread of this virus, allowing an early isolation of the infected patient [11].
Conflicts of interest: The authors certify that there is no conflict of interest with any financial organization regarding the material discussed in the manuscript. Funding: The authors report no involvement in the research by the sponsor that could have influenced the outcome of this work.
Authors’ contributions : All authors contributed equally to the manuscript and read and approved the final version of the manuscript.
#Human Metapneumovirus#sars cov 2#covid 19#jcrmhs#Journal of Clinical Case Reports Medical Images and Health Sciences quartile
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Authored by Martin Hoyt via RealClearHealth,
It did not have to be this way. The COVID-19 pandemic cost American citizens their lives, their livelihoods, education, mental health, reputations and, ultimately, civil and religious freedoms. “The U.S. accounts for less than 5% of the world’s population, but more than 25% of total COVID-19 cases reported across the globe, and it currently ranks among the top 10 countries in COVID-19-related deaths per capita,” wrote the authors of 2023 commentary in the Journal of the American Medical Association. And for all that, we have government to thank.
For years leading up to the pandemic, the nation had spent billions on preparation and planning for a biohazard attack or event. Whatever we learned was quickly discarded or undone by a lack of accountability, transparency, and humility. Decades of planning and untold man hours of research and training were rendered ineffective by a corrupt culture of greed, self-importance, scientific misconduct, and outright fraud. Because, while the government worked to prevent the worst, it was also helping to create chaos and contagion by funding and facilitating gain of function (GOF) research.
GOF research refers to laboratory efforts to make viruses deadlier or to increase their transmissibility. The potential for disaster is obvious. Almost five years prior to the pandemic Dr. Marc Lipsitch and Dr. Alison Galvani noted that GOF pathogenic research posed “a risk of accidental and deliberate release that, if it led to extensive spread of the new agent, could cost many lives … Furthermore, the likelihood of risk is multiplied as the number of laboratories conducting such research increases around the globe.”
But according to Dr. Anthony Fauci’s emails and other NIAID communications obtained via FOIA – those that weren’t deleted by the now-infamous “FOIA lady” – the Wuhan lab was working on Covid research with the U.S. as early as 2015. And the worst happened. Dr. Richard H. Ebright of Rutgers University told a Senate committee hearing on June 18, 2024, that “… lapses in U.S. oversight of gain-of-function research and enhanced potential pandemic pathogen research likely contributed to the origin of COVID-19 …”
While Ebright said GOF has no medical utility, he emphasized that there are “major incentives to researchers worldwide, in China, and in the U.S. The researchers undertake this research because it is easy, they get the money, and they can get the papers [in science journals].”
Not surprisingly, China was selected because it was quicker and cheaper to conduct research without U.S. government entanglements or oversight. Dr. Steven Quay also testified on June 18 and said the Wuhan Institute of Virology is a “level-2 lab,” as opposed to highly secure level-4 labs elsewhere. Moreover, Dr. Fauci et al were able to fund this research because the law was silent. Ebright again:
… in this category of research, which is the most significant in terms of consequences and potentially existential risk there is almost no regulation with force of law. No regulation with force of law for biosafety or any pathogen other than the smallpox virus and no regulation with force of law for bio risk management for any pathogen.
But the U.S. and the world, may have temporarily escaped imminent catastrophe. Consider, according to Dr. Quay, what Wuhan obtained from Canada’s National Microbiology Lab in 2019: “two vials each of 15 strains of virus: seven varieties of Ebola virus, the Hendra virus, and two strains of Nipah virus, Malaysia and Bangladesh.” These virus samples, according to Dr. Steven Quay, are “the top three most deadly human pathogens on the planet.” The samples were obtained under murky circumstances (“described as a possible policy breach”) from a level-4 lab and surreptitiously flown on a commercial flight to Beijing where they were subsequently placed in a level-2 lab overseen by a country with a long history of a disregard for proper safety protocols.
Gain of function research probably created COVID-19, but our legislative and executive branches created the conditions for the disaster. Congress failed to pass laws governing specific GOF research, both Congress and the executive branch failed to effectively manage the federal health and science bureaucracy, and various agencies failed to monitor the behavior and performance of grantees and vendors engaged in GOF research. When catastrophe struck, self-interest and political survival of those responsible overrode the best interests of our citizenry.
Who in the government benefited? How and to what extent did they benefit? Did any GOF research contribute to the U.S. global or response? Is GOF research being rerouted to our defense and security agencies to avoid scrutiny? NIAID continues to stall, obfuscate, and otherwise restrict transparency to its current and past activities. We know there was a concerted effort by senior leaders like Anthony Fauci to hide or delete emails but many other records still likely exist that remain uncovered.
This must change. Any research activity or sponsorship of scientific endeavors that are capable of mass extinction, such as GOF, must be subjected to a higher level of accountability and scrutiny by our elected leaders and the American public. Accountability, transparency, and public debate after an international crisis like Covid-19 can’t undo the global catastrophic harm that was done. It can, however, reduce the ability of our public health bureaucracy to contribute to the next disaster or looming crisis.
Borrowed from:
(https://stuff-that-irks-me.tumblr.com/)
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How can medicinal mushrooms support your mood and emotions?👀
[Hit SAVE so you can get these little miracle workers later!]
🍄Lion’s Mane: In a study of 30 women who were randomly assigned a snack of cookies containing Lion’s Mane or placebo cookies for 4 weeks, the Lion’s Mane group reported a significant reduction in feelings of helplessness, irritability and anxiety (Biomedical Research, 2010).
🍄Maitake: Researchers in 2017 found that Maitake had promising effects on mood and suggested it could be “a safe medical food supplement for the patient with depression” (Pharmaceutical Biology, 2017). This mushroom also acts as an adaptogenic food and can lower the stress hormone cortisol (Northern American Journal of Medical Sciences, 2011).
🍄Poria: Researchers in 2020 discovered that by calming the overreaction of the immune system and regulating our important neurotransmitters, including feel-good hormones serotonin and dopamine, Poria had a positive effect on mood. They also suggested that it could be “a traditional herbal
potential medicine for the treatment of depression.” (Journal of
Enthnopharmacology)
🍄Reishi: This powerful mushroom has been shown to reverse the decline in serotonin in the brain, meaning more of this happy hormone is circulating the brain to keep a positive mindset (Applied Microbiology and Biotechnology, 2021). Additionally, Reishi can help avoid low blood sugar, a common trigger for bad moods.
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Laboratory Based Non-Invasive Markers are Suboptimal in Detecting Advanced Fibrosis in Patients with Non-Alcoholic Steatohepatitis
Laboratory Based Non-Invasive Markers are Suboptimal in Detecting Advanced Fibrosis in Patients with Non-Alcoholic Steatohepatitis in Biomedical Journal of Scientific & Technical Research
Background and Aim: Hepatic fibrosis is a major determinant of clinical outcomes in patients with non-alcoholic steatohepatitis (NASH). We aimed to investigate the diagnostic performance of non-invasive tests in detecting advanced fibrosis (F3-4) in a large NASH cohort from central Ohio, the United States. Methods: Data of all patients with biopsy-proven NASH between 2014 and 2017 were collected. Diagnostic performance of aspartate aminotransferase (AST) to platelets ratio index (APRI), fibrosis-4 index (FIB-4) and NAFLD fibrosis score (NFS) were studied. Results: A total of 284 NASH patients were included, 27.82% of whom had F3-4. The cohort was predominantly female (60.92%) and White (88.38%) with a mean age of 50±13 years. The most common comorbidities were obesity (77.11%) and type 2 diabetes (49.65%). There was a significant difference in NFS between fibrosis stage F0-2 and F3-4 (-0.43±1.99 and 0.30±2.28, p=0.01). The sensitivity of APRI <1, FIB-4 <1.3, NFS <-1.455 were 28%, 64%, and 73.33%, respectively. The specificity of APRI ≥2, FIB-4 ≥3.25, NFS ≥0.675 were 93.1%, 84.73%, 74.26%, respectively. The negative predictive value of all three models ranged between 72.59% and 77.72%, and the positive predictive values were consistently low (<40.38%). The area under receiver operator curves of APRI, FIB-4, and NFS were 0.52, 0.55, and 0.59, respectively. Diagnostic performance of these models appeared to be better in older (>35 year) and male population. Conclusion: Overall APRI, FIB-4, NFS were suboptimal in detecting advanced fibrosis in our NASH cohort. Newer non-invasive tests with robust diagnostic accuracy are needed.
For more articles in Journals on Biomedical Sciences click here bjstr
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#medical and medicinal journal#american medical journal#journals on medical microbiology#biomedical open access journals#journals on medical informatics
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Scientists Offer a New Explanation for Long Covid (NYT)
"A team of scientists is proposing a new explanation for some cases of long Covid, based on their findings that serotonin levels were lower in people with the complex condition."
By Pam Belluck
Oct. 16, 2023
The News
A team of scientists is proposing a new explanation for some cases of long Covid, based on their findings that serotonin levels were lower in people with the complex condition.
In their study, published on Monday in the journal Cell, researchers at the University of Pennsylvania suggest that serotonin reduction is triggered by remnants of the virus lingering in the gut. Depleted serotonin could especially explain memory problems and some neurological and cognitive symptoms of long Covid, they say.
Why It Matters: New ways to diagnose and treat long Covid.
This is one of several new studies documenting distinct biological changes in the bodies of people with long Covid — offering important discoveries for a condition that takes many forms and often does not register on standard diagnostic tools like X-rays.
The research could point the way toward possible treatments, including medications that boost serotonin. And the authors said the biological pathway that their research outlines could unite many of the major theories of what causes long Covid: lingering remnants of the virus, inflammation, increased blood clotting and dysfunction of the autonomic nervous system.
“All these different hypotheses might be connected through the serotonin pathway,” said Christoph Thaiss, a lead author of the study and an assistant professor of microbiology at the Perelman School of Medicine at the University of Pennsylvania.
“Second of all, even if not everybody experiences difficulties in the serotonin pathway, at least a subset might respond to therapies that activate this pathway,” he said.
“This is an excellent study that identifies lower levels of circulating serotonin as a mechanism for long Covid,” said Akiko Iwasaki, an immunologist at Yale University. Her team and colleagues at the Icahn School of Medicine at Mount Sinai recently published a study that identified other biological changes linked to some cases of long Covid, including levels of the hormone cortisol. These studies could point to specific subtypes of long Covid or different biological indicators at different points in the condition.
The Back Story: A series of disruptions set off by bits of virus in the gut.
Researchers analyzed the blood of 58 patients who had been experiencing long Covid for between three months and 22 months since their infection. Those results were compared to blood analysis of 30 people with no post-Covid symptoms and 60 patients who were in the early, acute stage of coronavirus infection.
Maayan Levy, a lead author and assistant professor of microbiology at the Perelman School of Medicine, said levels of serotonin and other metabolites were altered right after a coronavirus infection, something that also happens immediately after other viral infections.
But in people with long Covid, serotonin was the only significant molecule that did not recover to pre-infection levels, she said.
The team analyzed stool samples from some of the long Covid patients and found that they contained remaining viral particles. Putting the findings in patients together with research on mice and miniature models of the human gut, where most serotonin is produced, the team identified a pathway that could underlie some cases of long Covid.
Here’s the idea: Viral remnants prompt the immune system to produce infection-fighting proteins called interferons. Interferons cause inflammation that reduces the body’s ability to absorb tryptophan, an amino acid that helps produce serotonin in the gut. Blood clots that can form after a coronavirus infection may impair the body’s ability to circulate serotonin.
Depleted serotonin disrupts the vagus nerve system, which transmits signals between the body and the brain, the researchers said. Serotonin plays a role in short-term memory, and the researchers proposed that depleted serotonin could lead to memory problems and other cognitive issues that many people with long Covid experience.
“They showed that one-two-three punch to the serotonin pathway then leads to vagal nerve dysfunction and memory impairment,” Dr. Iwasaki said.
There are caveats. The study was not large, so the findings need to be confirmed with other research. Participants in some other long Covid studies, in which some patients had milder symptoms, did not always show depleted serotonin, a result that Dr. Levy said might indicate that depletion happened only in people whose long Covid involves multiple serious symptoms.
What’s Next: A clinical trial of Prozac.
Scientists want to find biomarkers for long Covid — biological changes that can be measured to help diagnose the condition. Dr. Thaiss said the new study suggested three: the presence of viral remnants in stool, low serotonin and high levels of interferons.
Most experts believe that there will not be a single biomarker for the condition, but that several indicators will emerge and might vary, based on the type of symptoms and other factors.
There is tremendous need for effective ways to treat long Covid, and clinical trials of several treatments are underway. Dr. Levy and Dr. Thaiss said they would be starting a clinical trial to test fluoxetine, a selective serotonin reuptake inhibitor often marketed as Prozac, and possibly also tryptophan.
“If we supplement serotonin or prevent the degradation of serotonin, maybe we can restore some of the vagal signals and improve memory and cognition and so on,” Dr. Levy said.
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#لعاب الكلب قد يكون #قاتلا #نعلم طييا وبيولوجيا أن عضة الكلب تنقل للإنسان أمراضاً قد تنتهي بقطع رجله أو يده (مكان العضة). ولكن الدراسة الجديدة تحذر أن لعاب الكلب قد ينقل نفس البكتريا الخطيرة التي تتواجد في لعابه من خلال تربيته في المنزل والاقتراب منه كثيراً.. فالكلب يلعق جلد صاحبه تعاطفاً معه ولكن هذا الأمر قد ينقل أمراضاً خطيرة قد تنتهي بالموت! داء الكلب مسؤول عن موت 60000 إنسان سنوياً.. ولكن لعاب الكلب ملوث بشكل دائم بعدد من البكتريا الضارة والتي تنتقل للبشر عبر مداعبة الكلب أو تربيته وتقبيله.. مثلاً داء السلمونيلا Salmonellosis ينتقل بسهولة من الكلاب للبشر.. وهذا المرض له أعراض مثل التقيؤ وارتفاع درجة الحرارة وأعراض أخرى. تقول دراسة علمية نشرت في مجلة Journal of the Medical Association of Thailand بتاريخ ديسمبر 2003 : إن لعاب الكلب يحوي أكثر من 20 نوعاً من البكتريا.. دراسة أخرى نشرت في نوفمبر 2005 في مجلة Journal of Microbiology تؤكد وجود أنواع من البكتريا في لعاب الكلب مثل Actinomyces - Streptococcus - Granulicatella وأنواع أخرى. هناك كثير من الحالات التي انتهت بالموت على الرغم من عدم وجود عضة كلب، فقط مجرد المداعبة وترك الكلب يلعق أجزاء من وجه صاحبه ... قد تكون قاتلة بالفعل.. وهذا تقرير عن حالة وفاة لسيدة بسبب لعقة كلب! https://www.instagram.com/p/CpEAegisGJu/?igshid=NGJjMDIxMWI=
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New Study Reveals Hidden COVID Proteins in Blood of Long Haulers - Published Oct 21, 2024
A virus reservoir in the body may explain why some people experience long COVID symptoms.
A recent study indicates that long COVID sufferers with symptoms impacting multiple body systems might have persistent SARS-CoV-2 proteins in their blood, pointing to an ongoing viral infection that could be treated with antivirals.
Persistent Viral Proteins in Long COVID Patients A study conducted by Harvard-affiliated Brigham and Women’s Hospital revealed that individuals experiencing a broad array of long COVID symptoms are twice as likely to have traces of SARS-CoV-2 proteins in their blood compared to those without symptoms of long COVID.
The symptoms frequently associated with long COVID include fatigue, brain fog, muscle and joint pain, back pain, headaches, sleep issues, loss of smell or taste, and gastrointestinal problems.
These findings were published in the journal Clinical Microbiology and Infection.
Implications for Long COVID Treatment Strategies Specifically, the team found that 43 percent of those with long COVID symptoms affecting three major systems in the body, including cardiopulmonary, musculoskeletal, and neurologic systems, tested positive for viral proteins within 1 to 14 months of their positive COVID test. But only 21 percent of those who didn’t report any long COVID symptoms tested positive for the SARS-CoV-2 biomarkers in this same period.
“If we can identify a subset of people who have persistent viral symptoms because of a reservoir of virus in the body, we may be able to treat them with antivirals to alleviate their symptoms,” said lead author Zoe Swank, a postdoctoral research fellow in the Department of Pathology at BWH.
Insights From the RECOVER Initiative The study analyzed 1,569 blood samples collected from 706 people, including 392 participants from the National Institutes of Health-supported Researching COVID to Enhance Recovery (RECOVER) Initiative, who had previously tested positive for a COVID infection. Using Simoa, an ultrasensitive test for detecting single molecules, researchers looked for whole and partial proteins from the SARS-CoV-2 virus. They also analyzed data from the participants’ long COVID symptoms, using electronic medical chart information or surveys that were gathered at the same time as the blood samples were taken.
It’s possible that a persistent infection explains some — but not all — of the long COVID sufferers’ symptoms. If this is the case, testing and treatment could aid in identifying patients who may benefit from treatments such as antiviral medications.
The Complex Nature of Long COVID One of the questions raised by the study is why more than half of patients with wide-ranging long COVID symptoms tested negative for persistent viral proteins.
“This finding suggests there is likely more than one cause of long COVID,” said David Walt, a professor of pathology at BWH and principal investigator on the study. “For example, another possible cause of long-COVID symptoms could be that the virus harms the immune system, causing immune dysfunction to continue after the virus is cleared.”
To better understand whether an ongoing infection is behind some people’s long COVID symptoms, Swank, Walt, and other researchers are currently conducting follow-up studies. They’re analyzing blood samples and symptom data in larger groups of patients, including people of wide age ranges and those with compromised immune symptoms. This way, they can also see if some people are more likely to have persistent virus in the body.
“There is still a lot that we don’t know about how this virus affects people,” said David C. Goff, a senior scientific program director for the RECOVER Observational Consortium Steering Committee and director of the Division of Cardiovascular Sciences at the National Heart, Lung, and Blood Institute (NHLBI), part of NIH. “These types of studies are critical to help investigators better understand the mechanisms underlying long COVID — which will help bring us closer to identifying the right targets for treatment.”
Goff added that these results also support ongoing efforts to study antiviral treatments.
The SARS-CoV-2 blood test developed by Brigham and Women’s researchers is also currently being used in a national study, called RECOVER-VITAL, that is testing whether an antiviral drug helps patients recover from long COVID. The RECOVER-VITAL trial will test the patients’ blood before and after treatment with an antiviral to see if treatment eliminates persistent viral proteins in the blood.
The idea that a virus can stay in the body and cause ongoing symptoms months after an infection isn’t unique to COVID.
“Other viruses are associated with similar post-acute syndromes,” said Swank. She noted animal studies have found Ebola and Zika proteins in tissues post-infection, and these viruses have also been associated with post-infection illness.
Reference: “Measurement of circulating viral antigens post-SARS-CoV-2 infection in a multicohort study” by Zoe Swank, Ella Borberg, Yulu Chen, Yasmeen Senussi, Sujata Chalise, Zachary Manickas-Hill, Xu G. Yu, Jonathan Z. Li, Galit Alter, Timothy J. Henrich, J. Daniel Kelly, Rebecca Hoh, Sarah A. Goldberg, Steven G. Deeks, Jeffrey N. Martin, Michael J. Peluso, Aarthi Talla, Xiaojun Li, Peter Skene, Thomas F. Bumol and Mike Zissis, 9 October 2024, Clinical Microbiology and Infection. DOI: 10.1016/j.cmi.2024.09.001
www.clinicalmicrobiologyandinfection.com/article/S1198-743X(24)00432-4/abstract (PAYWALLED)
#mask up#covid#pandemic#wear a mask#public health#wear a respirator#covid 19#still coviding#coronavirus#sars cov 2#long covid#covid is not over#covid conscious
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🍄 Embarking on the Enigmatic Journey of Kingdom Fungi🍄
Greetings, curious minds! Today, let's unravel the intricacies of Kingdom Fungi, a fascinating realm teeming with diversity and significance. 🧫🌐
1. Morphological Marvels:
At the heart of fungal wonders lies an array of captivating structures. From the towering mushrooms in our forests to the microscopic threads known as hyphae, fungi showcase an unparalleled morphological diversity. Join me as we delve into the labyrinthine world of mycelium, sporangia, and spores, where each component plays a crucial role in their life cycle and ecological impact. 🕵️♂️🔬
2. Ecological Ballet:
Picture the dance of fungi in the grand theater of ecosystems. As decomposers, fungi break down organic matter, recycling nutrients and sustaining life cycles. But their role extends beyond, as mycorrhizal partnerships with plants reveal a harmonious interdependence. Together, let's explore how fungi shape the intricate tapestry of ecological balance and contribute to the health of our planet. 🌱🍂🔄
3. Pathogenic Prowess:
Venture into the shadows where fungi wield their pathogenic powers. Discover the intricacies of fungal infections in humans, plants, and animals. How do these formidable foes infiltrate our defenses, and what strategies do they employ to thrive in their chosen hosts? Uncover the mysteries of fungal pathogenicity and the ongoing battle between host and invader. 💉🦠
References:
1. Hawksworth, D. L. (2001). The magnitude of fungal diversity: The 1.5 million species estimate revisited. Mycological Research, 105(12), 1422-1432.
2. Blackwell, M. (2011). The fungi: 1, 2, 3... 5.1 million species? American Journal of Botany, 98(3), 426-438.
3. Tortorano, A. M., et al. (2014). European Confederation of Medical Mycology (ECMM) epidemiological survey on invasive infections due to Fusarium species in Europe. European Journal of Clinical Microbiology & Infectious Diseases, 33(1), 1623-1630.
Embrace the fungal odyssey! 🌐🔍
#science#biology#college#education#school#student#medicine#doctors#health#healthcare#wild fungi#fungi
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Grant Medical College: A Legacy of Medical Excellence
Located in Mumbai, Maharashtra, Grant Medical College (GMC) is one of the oldest and most prestigious medical institutions in India. Founded in 1845, GMC has a rich history and has consistently maintained a reputation for excellence in medical education and healthcare services. It is affiliated with the Maharashtra University of Health Sciences (MUHS) and works with the renowned Professor Sir J.J. Hospitals, providing students with valuable clinical and hands-on experience.
Historical Significance:
The establishment of Grant Medical College marked a turning point in medical education in India as it was the first time a formal medical curriculum was offered in the region. Named after the then Governor of Bombay, Sir Robert Grant, GMC was established to cater to the growing demand for medical professionals in India. Over the years, it has produced a large number of outstanding graduates who have made significant contributions to the medical field both at home and abroad.
Academic Programmes and Specialisations:
GMC offers undergraduate (MBBS) and postgraduate programs in a wide range of specializations including Surgery, Paediatrics, Radiology, Gynaecology, etc. The college admits around 200 MBBS students every year, who are selected through a competitive admission process. Postgraduate courses are also in high demand and provide advanced training in over 20 subject areas. The courses are designed to not only impart medical knowledge but also develop students' critical thinking and problem-solving skills, preparing them for real-world medical challenges.
Curriculum and Training:
The curriculum at GMC is comprehensive, combining theoretical knowledge with practical skills. Students receive extensive clinical training and encounter a wide range of medical cases and complex surgeries. Access to Sir J.J. Hospital, a large tertiary care hospital, allows students to work with experienced doctors and interact with patients from a variety of backgrounds. This hands-on training gives them a realistic and in-depth understanding of healthcare.
Grant Medical College also values research and innovation and encourages students and faculty to get involved in clinical research projects. The university has a research center that promotes research in areas such as pathology, microbiology, pharmacy, and public health. The strong focus on research enriches the student's learning experience and keeps abreast of advancements in the medical field.
Faculty and Infrastructure:
GMC has highly qualified and experienced faculty members who are dedicated to serving students. Many faculty members are recognized experts in their fields, having published papers in medical journals and participated in conferences across the world. Their expertise ensures that students receive a quality education backed by practical insights.
GMC's infrastructure is also noteworthy. With modern laboratories, a large, well-resourced library, lecture halls, and digital learning facilities, the college offers an ideal environment for medical training. Its affiliated Sir J.J. Hospital functions as a teaching hospital, providing quality medical services and facilities for both patients and students.
Campus Life and Student Activities:
GMC is known for its academic rigor, but it also encourages students to get involved in extracurricular activities. The college has a variety of student organizations and clubs that focus on sports, cultural events, and community service. The annual GMC festival, known as Astitva, is a much-anticipated event where students showcase their talents and take part in various competitive activities. This balance of academics and extracurricular activities contributes to the holistic development of students, preparing them to become well-rounded medical professionals.
Employment and Career Outlook:
Grant Medical College graduates enjoy a high employment rate, securing many prestigious positions in leading hospitals and medical institutions in India and abroad. The college's reputation and strong alumni network provide excellent career opportunities. GMC graduates hold key positions in healthcare institutions, research institutes, and academia across the globe. Many of our graduates pursue further specializations, research careers or participate in public health efforts.
Conclusion:
Grant Medical College is a pillar of medical education in India. With its tradition of producing qualified medical professionals and commitment to quality education, GMC continues to be a preferred choice for aspiring doctors. A combination of academic excellence, practical training, and a rich historical background makes it a reputed institution driving the future of healthcare in India.
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