Stretch the shelf-life of your grapes with these tips.

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No matter the variety, grapes make for a delicious snack, especially when theyre spread across a beautiful charcuterie board (theyre of course also delicious in liquid form, if you catch my drift). But grapes also happen to be a pricier produce item, and can spoil quite quickly if not stored properly. It can also be difficult to pick the perfect bunch of grapes since theyre so tightly clustered together.

Still, there are a few things to look out for when examining grapes at the grocery store. Its always important to make sure theyre firm, plump, and attached to the stem. If you pick up a bag with loose grapes rolling around at the bottom, thats a good indicator that they may be quicker to spoil. And while this may seem like common knowledge, you should also avoid grapes that are moldy, watery, and shriveled at the stem. However, if you see a whiteish coating on a bunch of grapes, thats totally fine. Its called bloom, which is a naturally occurring substance that protects grapes from moisture loss.

:13 Foods That (Basically) Never Spoil

Now that you know how to pick out a stellar bunch, keep reading for tips on how to store grapes so you can enjoy them for weeks at a time.

Have you ever walked into someones kitchen and noticed a big, beautiful bowl of grapes on the counter? While grapes may make for a convenient grab-and-go snack when stored this way, this is the quickest way for grapes to lose their moisture and crispness.

Instead, whole grapes should be washed, patted dry, and then stored in a well-ventilated container in the crisper drawer of your refrigerator. This will allow them to last for up to three weeks. Youll want to avoid putting them into an airtight container or plastic bag, since that prevents air circulation. You could also keep whole grapes in the bag they came in if you dont have a proper food storage container.

:How to Store Strawberries So They Won't Spoil Quickly

If you have leftover cut up grapes, theres no need to toss them just yet! Cut grapes can be stored in an airtight container in the refrigerator for up to 48 hours. If you notice the edges start to dry up and brown, thats finetheyre still safe to eat.

Use any leftover cut grapes as a yogurt or oatmeal topping, or as a bite-sized snack.

Yes, you can freeze grapes. And if youve never had frozen grapes, what are you waiting for?! They make for such a quick and delicious snack or dessertbasically like an all-natural, bite-sized freeze pop.

:Does Flour Go Bad? Here's When You Should Replace Your Baking Staples

To freeze, simply rinse and dry your grapes and spread them out on a lined baking sheet. Place them in the freezer for a few hours or overnight, and once theyre frozen, you can put them in a storage container so theyre easily accessible. Just make sure that your grapes arent clumped together on the baking sheet, otherwise they will freeze together (which I guess isnt the worst thing). If youre feeling especially fancy, you can roll your frozen grapes in coarse sugar to add some extra sweetness. Just make sure you enjoy them immediately!

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How to Store Grapes So They Stay Firm and Fresh - AOL

William Haseltine

It is becoming increasingly clear that we have misunderstood SARS-CoV-2, the virus that causes COVID-19. Many people, including some experts in the scientific community, deemed the pandemic over with the release of the mRNA vaccines. The beliefor perhaps it was hope in disguisewas that with the development of the vaccines, we could go back to living our lives as usual, back to a semblance of pre-pandemic normalcy. This simply is not so, as evidenced by surging cases around the world and the continued onslaught of variant after variant.

Even the latest approach, trying to play catch-up with variants by updating our vaccines to match the dominant circulating strain, is a losing game; we will always be one step behind, forced to adapt to the cards we are dealt rather than dictating the playing field. This should come as no surprise. Across the globe, highly skilled influenza researchers have been battling for decades to develop long-lasting, broadly neutralizing flu shots. Although plenty of progress has been made, we still have yearly flu seasons, some of which are plagued by low vaccine efficacyin 2021/2022, the vaccine was only 36% effective at preventing influenza cases requiring medical attention.1

At this point, we seem to have accepted that we will be living with COVID-19 for the foreseeable future; such complacency is very dangerous. Living with the virus is no different from living with a pet lion; there is never any guarantee of safety. We know SARS-CoV-2 can change rapidly, we know it can become far more virulent, and we have no idea of the determinants of pathogenesis.

Our single-minded reliance on vaccines, at the expense of developing novel drug therapies, has left us fighting with one hand tied behind our back. Our current antivirals are anemic at best: they are either no longer effective, like most monoclonal antibodies, or they simply cannot prevent infection in the first place. If we ever hope to control COVID-19, we need to join the battle fully. This means a dramatic increase in resources to fund drug development efforts. The problem is not a lack of tools; it is a lack of political, scientific, and economic will. It is time to change that.

What follows is a summary of the shortcomings of our currently available antiviral drugs as well as a brief overview of some promising, up-and-coming contenders.

1. Monoclonal Antibodies (mAbs)

Monoclonal antibodies are antibodies designed to target a specific antigen or even a specific region of an antigen, usually the spike protein. Once the antibodies bind to the antigen, they either block it from being able to bind to our cells or mark it for destruction by other immune cells. As such, they work well in instances where they correctly match up to the antigen at handsuccessfully neutralizing the virus and inhibiting infectionbut suffer from the same major issues as vaccines: viral resistance and viral mutation.2 With repeat or extended exposure to a certain antibody, SARS-CoV-2 will eventually mutate to escape the immune system, rendering the antibody ineffective and even in the absence of resistance, run-of-the-mill viral mutation can have the same effect.

Monoclonal antibodies come with the additional drawback of needing to be administered intravenously or subcutaneously by a healthcare professional. None of the currently available options come in an oral format, as a pill. This means people with mild-to-moderate diseasenot bad enough to warrant hospitalizationoften do not receive treatment and, while sick, run the risk of infecting others. Practically speaking, monoclonal antibodies simply cannot be used prophylactically; they may help you once youre in the hospital, but they wont be able to stop you from ending up there in the first place.

2. Paxlovid

Paxlovid is a kinase inhibitor that interferes with the main protease (Mpro) of SARS-CoV-2; it is highly efficacious, safe, and is taken orally. Early clinical trial results confirmed its promise, indicating a near-90% reduction in the risk of COVID-19related hospitalizations and deaths.3 Even in a highly vaccinated population, the drug was able to reduce hospitalization or death by 44% in adults over 50 years of age.4 And unlike monoclonal antibodies, viral resistance and viral variation pose less of an issue for Paxlovid because the main protease is a highly conserved region of the SARS-CoV-2 genome. Whereas the spike protein can undergo large structural changes without too heavy of a sacrifice on viral fitness, this is simply not true of the main protease.5

So what are the drawbacks? First on the list is a phenomenon that has been termed Paxlovid rebound. This occurs when, following a full course of the medication and apparent clearance of the virus, symptoms suddenly return. Although this may happen even in the absence of antiviral treatmentsone preprint indicates that up to 10% of infections are followed by a rebound in symptoms and 12% by a rebound in viral levels it is more common in those treated with Paxlovid.6,7 The main limitation facing Paxlovid, however, is its inability to prevent infection.8 As such, it cannot be used in a pre- or post-exposure context, cannot avert onward transmission, and cannot contain the pandemic. It is a great start and points us in the right direction, but it is not the final solution.

3. Remdesivir

Remdesivir is a nucleoside analogue that works by inhibiting RNA-dependent RNA polymerasethe enzyme that builds up viral RNA chains during replication. Despite being a nucleotide analogue, it does not carry the mutagenic risk of molnupiravir; rather than being incorporated into the viral genome and then introducing errors, it works by being incorporated into the viral genome and then stalling the inclusion of any additional nucleosides.

Still, remdesivir suffers from other issues. First and foremost is the problem of low efficacy. Results from the World Health Organization (WHO) Solidarity Trial, a randomized trial that enlisted roughly 3,000 people, concluded that remdesivir has no significant effect on patients with COVID-19 who are already being ventilated.9 For hospitalized patients not requiring ventilation, remdesivir had only a small, nonsignificant effect on death or progression to ventilation.

Another major drawback of remdesivir is the fact it must be administered intravenously across the span of multiple days. As with monoclonal antibodies, this significantly limits its practicality for everyday use. It also means that it cannot be used in a prophylactic capacity.

4. Molnupiravir

Molnupiravir works by inserting errors into the viral genome.10 These errors are then copied during replication, and when enough of them accrue, viral proteins end up with too many mutations to properly function, incapacitating the virus. The main issue facing molnupiravir is low efficacy. It was initially touted to reduce the risk of hospitalization and death by up to 50%, but this number dropped down to 30% by the end of the full clinical trial.11,12 Since then, new data from the largest randomized trial of molnupiravir, which enlisted a total of 26,000 individuals, indicate that molnupiravir offers no reduction in the frequency of COVID-19associated hospitalizations or deaths in high-risk vaccinated adults.13 Whether you take molnupiravir or you take a placebo, your odds are the same.

The low efficacy is further problematized by a dubious safety profile. Owing to a shared intermediate required in both the synthesis of viral RNA as well as human DNAribonucleoside 5-diphosphatemolnupiravir may pose a mutagenic threat to humans: instead of introducing errors only to viral RNA, the drug may also lead to host DNA mutations.14 Long term, this could result in the growth of cancerous tumors and even birth defects, either through mutated sperm precursor cells or if given directly to pregnant women.

Molnupiravirs mechanism of action also carries the risk of spawning new viral variants. Recall that its entire modus operandi is, essentially, destruction via mutation. Certain scenarios, some as banal as a person forgetting to finish their full course of medication, may bring about all of the mutation with none of the destruction. The risk of such viral mutations following treatment with molnupiravir is especially acute in immunocompromised patients, where new variants can form as quickly as a day or two.15

New Drugs, Familiar Mechanisms

Many of the novel COVID-19 drugs making their way through the development and trial pipeline are based on the same broad strategies as the antivirals discussed above. They take advantage of the same viral weaknesses but try to improve on the limitations of their predecessors.

Take, for example, the kinase inhibitor Xocova. Developed by Japanese pharmaceutical company Shionogi, it works in the same way as Paxlovid, by inhibiting the main protease (Mpro) of SARS-CoV-2. Early efficacy data, albeit based on a very small sample size, indicates robust antiviral activity, with a rapid decrease in viral RNA titers compared with placebo.16 That said, time until relief of symptoms was similar between the two groups.

Another group of Japanese researchers developed and tested main protease inhibitors that include fluorine atoms to increase cell membrane permeability and binding affinity for the pocket of Mpro. The team also replaced the digestible amide bond with a surrogate structure to improve biostability. The modified compounds outperformed nirmatrelvir in mouse models.17

Then there is VV116, an oral remdesivir derivative.18 Like its parent compound, it works by inhibiting the RNA-dependent RNA polymerase. Unlike its parent compound, however, VV116 matches Paxlovid in efficacy, enabling clinical recovery from mild-to-moderate COVID-19 in the same amount of time.19 And crucially, where remdesivir must be delivered via injection or intravenous drip, VV116 can be taken orally, expanding its potential reach.

Despite small improvements, such up-and-coming antivirals represent a mostly lateral move. True, they expand our arsenal of treatments against COVID-19 and help decrease the risk of viral resistance, but ultimately they differ from our current antivirals in degree, not in kind. Like Paxlovid, molnupiravir, monoclonal antibodies, and remdesivir, none of them will work prophylacticallythey can only treat, not prevent.

Exploiting Vulnerabilities: Strategies for Prophylactic Drug Design

With an eye toward prevention, its clear we need to diversify our lines of attack against SARS-CoV-2. What follows is a broad overview of strategies that may yield more success in the pursuit of prophylactic antivirals.

COVID-19 begins when SARS-CoV-2 first encounters cells in the upper airway that express a suitable attachment site, the angiotensin converting enzyme 2 (ACE 2). But entry into the target cells requires much more than surface attachment; after the virus has attached itself to ACE2, it still needs to fuse with the host cell membrane in order to inject its genetic material into the cytoplasm, where replication can begin. To fuse with the host membrane, SARS-CoV-2 depends on certain human enzymesfurin, transmembrane serine proteases (TMPRSSs), and cathepsins (CTSs)to cleave its spike (S) protein. Inhibition of ACE2-binding or of membrane fusion blocks viral entry, short circuiting infection before it ever gets a foothold.

Binding and fusion are complex processes with many moving parts, rendering them sites of potential failure. Scientists have begun exposing these vulnerabilities and leveraging them to their advantage.

1. Potential therapies targeting the human ACE2 receptor of the viral spike protein

A massive survey of 2,900 FDA-approved drugs revealed that carvedilol, a beta blocker used to treat high blood pressure and heart failure, may also prove useful against SARS-CoV-2.20 To test its suitability, researchers exposed human lung cells (A549-ACE2) to carvedilol for two hours before infecting them with SARS-CoV-2. After two days of incubation, they checked the cells for the presence of SARS-CoV-2 spike protein, used as a marker of infection. At a half-maximal effective concentration of 4.1M, carvedilol successfully cleared infection. Further, assessment of two large COVID-19 databases indicated that carvedilol-use was associated with a 17% lower risk of a COVID-19 positive test result. Although the exact mechanism of action through which carvedilol inhibits SARS-CoV-2 entry into cells is unknown, the researchers suggest this may happen through disruption of spike proteinACE2 interactions.

Another candidate, aloperine, comes by way of a medicinal plant called Sophora alopecuroides L. Isolated from the seeds of the plant, aloperine and its various derivatives have previously been shown to impair viral entry of HIV-1 and influenza.21 A recent study indicates that aloperines antiviral activity extends to SARS-CoV-2, successfully inhibiting entry into host cells in vitro.22 Compound 5, one of many aloperine-derivatives, proved especially effective, capable of limiting viral entry not only against pseudotyped viruses with the D614G variant of the spike protein, but also against Delta and Omicron variants. Confocal microscopy suggests that compound 5 inhibits viral entry before fusion to the cell or endosomal membrane.

Then there are a variety of ACE2 decoys, which mimic the receptor protein and trick the virus into binding to them instead of binding the real thing.23 Once the SARS-CoV-2 spike protein binds to the decoy, it undergoes irreversible structural changes that prevent it from being able to bind to ACE2 down the line, effectively blocking viral entry. ACE2 decoys come with the added benefit of being broadly-neutralizing; whereas SARS-CoV-2 evolves to escape monoclonal antibodies, evolution selects for ACE2 affinity. Thus, viral resistance to ACE2 decoys would come at the expense of its ability to bind ACE2, impairing infectivity and overall viral fitness. ACE2 decoys remain effective against the Omicron family of SARS-CoV-2.

2. Therapies targeting viral membrane fusion

In addition to fusing with the cell membrane directly, SARS-CoV-2 can inject its genetic material into cells by being absorbed into the cell in a vesicle, a process known as endocytosis, and then fusing with the membrane of the endosome once inside the cell. Obatoclax, an experimental drug for the treatment of cancers, was found to deliver a double strike against SARS-CoV-2, blocking both direct membrane fusion as well as endocytosis; it blocks direct membrane fusion by reducing furin activity and it blocks endocytosis by reducing the activity of cathepsin L.24 In vitro, obatoclax retained its potency against the spike proteins of different variants, including Alpha, Beta, and Delta. The study was performed prior to the emergence of Omicron.

An additional approach to blocking cathepsin Lmediated entry of SARS-CoV-2 involves the use of the RNA-editing tool Genome-wide Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)-Cas13. With the help of CRISPR-Cas13, researchers knocked down cathepsin L messenger RNA (mRNA) in the lungs of mice, significantly reducing viral entry.25 To deliver the CRISPR-Cas13 specifically to the lungsleaving cathepsin L untouched in the spleen and the liverthey engineered lung-selective lipid nanoparticles (LNPs). Both prophylactic and therapeutic administration of the lung-specific CRISPR-Cas13dbased therapy effectively inhibits lethal SARS-CoV-2 infection in mice. Significantly, this approach inhibited infection not only against wild-type SARS-CoV-2 and against the Delta variant, but also against SARS-CoV-1, the cause of the 2003 SARS outbreak.

Cathepsin L is one of the two main proteases that SARS-CoV-2 depends on for viral entry into host cells. The other, as mentioned above, is TMPRSS2. A group of German scientists tested nafamostat mesylate, a kinase inhibitor that targets TMPRSS2 and is approved for treatment of pancreatitis in Japan, for its ability to block SARS-CoV-2 infection. Indeed, the compound strongly suppressed viral entry in vitro.26 A separate study, using kinase inhibitors to simultaneously block TMPRSS2 and cathepsin B, yielded similar results, with a reduction of viral load to 0.036% in ACE2-expressing human induced pluripotent stem cells.27 These results held up against multiple variants.

As much as we would like to pretend otherwise, the COVID-19 pandemic does not end where vaccines begin. At least not the current vaccines. XBB.1.5 is just the latest reminder that, as long as SARS-CoV-2 continues to spread and mutate we will continue to see waves of infection.

This is not to say that vaccines do not have their place in the fight against COVID-19, they clearly do, but rather that they are not the panacea that many hoped and that some claimed they would be. Vaccination is one protective strategy, but we cannot put all of our eggs in a single basket. And if we do, we should not be surprised when they end up cracking. Vaccines protect against the worst of COVID-19, but they do so only for a limited duration and against a limited number of variants. This wont change anytime soon.

What can we do to help improve our odds against SARS-CoV-2? We need to actively expand our arsenal of anti-COVID-19 drugs. In particular, it should have dawned on us that we need to develop combinatorial drug therapies that can be used prophylactically, to prevent infection and stop onward transmission. We still do not have a vaccine for human immunodeficiency virus (HIV), for example, but new infections and deaths continue to decline.28 We owe this largely to antiretroviral therapy (ART) and pre-exposure prophylactic (PrEP) medication. Antiretrovirals help those who are HIV positive suppress viral loads to undetectable levels. Undetectable = untransmittable, meaning they cannot pass the virus on to others.29 Similarly, pre-exposure prophylactic (PrEP) medication helps protect those at high-risk of exposure to HIV. As long as it is taken as prescribed, it prevents the virus from taking hold in the body.

If we hope to ever contain SARS-CoV-2, we need to pursue a similar strategy. My recommendation is the following: in the United States, a warp-speed-like project between government, industry, and academia and a minimum of five billion, or up to ten billion, additional dollars per year to fund such collaborations.30 A similar commitment to public health and drug development must be echoed by others, especially the European Union and China. We also need to make sure we have global clinical trial capabilities in place, so that wherever outbreaks occur, we are prepared to test novel drugs on the spot. It is time to fight the battle with both hands, not just one.

References

William R. Haseltine, PhD, is chair and president of the think tank ACCESS Health International, a former Harvard Medical School and School of Public Health professor and founder of the universitys cancer and HIV/AIDS research departments. He is also the founder of more than a dozen biotechnology companies, including Human Genome Sciences.

Read more here:
Can We Still Contain, and Possibly Eliminate, COVID-19? Yes, and ... - Inside Precision Medicine

What is positron emission tomography (PET)?

Positron emission tomography (PET) is a type of nuclear medicine procedure that measures metabolic activity of the cells of body tissues. PET is actually a combination of nuclear medicine and biochemical analysis. Used mostly in patients with brain or heart conditions and cancer, PET helps to visualize the biochemical changes taking place in the body, such as the metabolism (the process by which cells change food into energy after food is digested and absorbed into the blood) of the heart muscle.

PET differs from other nuclear medicine examinations in that PET detects metabolism within body tissues, whereas other types of nuclear medicine examinations detect the amount of a radioactive substance collected in body tissue in a certain location to examine the tissue's function.

Since PET is a type of nuclear medicine procedure, this means that a tiny amount of a radioactive substance, called a radiopharmaceutical (radionuclide or radioactive tracer), is used during the procedure to assist in the examination of the tissue under study. Specifically, PET studies evaluate the metabolism of a particular organ or tissue, so that information about the physiology (functionality) and anatomy (structure) of the organ or tissue is evaluated, as well as its biochemical properties. Thus, PET may detect biochemical changes in an organ or tissue that can identify the onset of a disease process before anatomical changes related to the disease can be seen with other imaging processes such as computed tomography (CT) or magnetic resonance imaging (MRI).

PET is most often used by oncologists (doctors specializing in cancer treatment), neurologists and neurosurgeons (doctors specializing in treatment and surgery of the brain and nervous system), and cardiologists (doctors specializing in the treatment of the heart). However, as advances in PET technologies continue, this procedure is beginning to be used more widely in other areas.

PET may also be used in conjunction with other diagnostic tests, such as computed tomography (CT) or magnetic resonance imaging (MRI) to provide more definitive information about malignant (cancerous) tumors and other lesions. Newer technology combines PET and CT into one scanner, known as PET/CT. PET/CT shows particular promise in the diagnosis and treatment of lung cancer, evaluating epilepsy, Alzheimer's disease and coronary artery disease.

Originally, PET procedures were performed in dedicated PET centers, because the equipment to make the radiopharmaceuticals, including a cyclotron and a radiochemistry lab, had to be available, in addition to the PET scanner. Now, the radiopharmaceuticals are produced in many areas and are sent to PET centers, so that only the scanner is required to perform a PET scan.

Further increasing the availability of PET imaging is a technology called gamma camera systems (devices used to scan patients who have been injected with small amounts of radionuclides and currently in use with other nuclear medicine procedures). These systems have been adapted for use in PET scan procedures. The gamma camera system can complete a scan more quickly, and at less cost, than a traditional PET scan.

PET works by using a scanning device (a machine with a large hole at its center) to detect photons (subatomic particles) emitted by a radionuclide in the organ or tissue being examined.

The radionuclides used in PET scans are made by attaching a radioactive atom to chemical substances that are used naturally by the particular organ or tissue during its metabolic process. For example, in PET scans of the brain, a radioactive atom is applied to glucose (blood sugar) to create a radionuclide called fluorodeoxyglucose (FDG), because the brain uses glucose for its metabolism. FDG is widely used in PET scanning.

Other substances may be used for PET scanning, depending on the purpose of the scan. If blood flow and perfusion of an organ or tissue is of interest, the radionuclide may be a type of radioactive oxygen, carbon, nitrogen, or gallium.

The radionuclide is administered into a vein through an intravenous (IV) line. Next, the PET scanner slowly moves over the part of the body being examined. Positrons are emitted by the breakdown of the radionuclide. Gamma rays called annihilation photons are created when positrons collide with electrons near the decay event. The scanner then detects the annihilation photons, which arrive at the detectors in coincidence at 180 degrees apart from one another. A computer analyzes those gamma rays and uses the information to create an image map of the organ or tissue being studied. The amount of the radionuclide collected in the tissue affects how brightly the tissue appears on the image, and indicates the level of organ or tissue function.

In general, PET scans may be used to evaluate organs and/or tissues for the presence of disease or other conditions. PET may also be used to evaluate the function of organs, such as the heart or brain. The most common use of PET is in the detection of cancer and the evaluation of cancer treatment.

More specific reasons for PET scans include, but are not limited to, the following:

To diagnose dementias (conditions that involve deterioration of mental function), such as Alzheimer's disease, as well as other neurological conditions such as:

Parkinson's disease. A progressive disease of the nervous system in which a fine tremor, muscle weakness, and a peculiar type of gait are seen.

Huntington's disease. A hereditary disease of the nervous system which causes increasing dementia, bizarre involuntary movements, and abnormal posture.

Epilepsy. A brain disorder involving recurrent seizures.

Cerebrovascular accident (stroke)

To locate the specific surgical site prior to surgical procedures of the brain

To evaluate the brain after trauma to detect hematoma (blood clot), bleeding, and/or perfusion (blood and oxygen flow) of the brain tissue

To detect the spread of cancer to other parts of the body from the original cancer site

To evaluate the effectiveness of cancer treatment

To evaluate the perfusion (blood flow) to the myocardium (heart muscle) as an aid in determining the usefulness of a therapeutic procedure to improve blood flow to the myocardium

To further identify lung lesions or masses detected on chest X-ray and/or chest CT

To assist in the management and treatment of lung cancer by staging lesions and following the progress of lesions after treatment

To detect recurrence of tumors earlier than with other diagnostic modalities

Read the original here:
Positron Emission Tomography (PET) | Johns Hopkins Medicine

pet, any animal kept by human beings as a source of companionship and pleasure.

While a pet is generally kept for the pleasure that it can give to its owner, often, especially with horses, dogs, and cats, as well as with some other domesticated animals, this pleasure appears to be mutual. Thus, pet keeping can be described as a symbiotic relationship, one that benefits both animals and human beings. As the keeping of pets has been practiced from prehistoric times to the present and as pets are found in nearly every culture and society, pet keeping apparently satisfies a deep, universal human need.

The history of pets is intertwined with the process of animal domestication, and it is likely that the dog, as the first domesticated species, was also the first pet. Perhaps the initial steps toward domestication were taken largely through the widespread human practice of making pets of captured young wild animals. Eventually, a working relationship developed between the dogs and their human captors. The dog was swifter, had stronger jaws, and was better at tracking prey; therefore, it could be of great use in hunting and guarding duties. From human beings, on the other hand, the dogs were assured of a constant supply of food as well as warmth from the fire. There is indirect evidence that the dog may have been domesticated and kept as a pet since Paleolithic times, as can be surmised from the paintings and carvings that archaeologists have found in ancient campsites and tombs. In Mesopotamia, dogs that look remarkably like the present-day mastiff were shown participating in a lion hunt. Domestic pets were often depicted in the scenes of family life in ancient Egypt; hunting dogs of the greyhound or saluki type accompany their master to the chase, and lap dogs frequently sit under the chair of their master or mistress.

Next to the dog, horses and cats are the animals most intimately associated with human beings. Surprisingly, both these animal groups were domesticated rather late in human history. There is no evidence that horses were domesticated in Paleolithic or Mesolithic times, but by about 2000 bce horses used in chariot battles were an established phenomenon throughout the Middle East. It seems that riding astride horses was a practice developed a few centuries later (see horsemanship). The cat too does not seem to have been domesticated as a pet until the New Kingdom period (about the 16th century bce) in Egypt. This is all the more strange as the ancient Egyptians had tamed many types of animals, such as lions, hyenas, monkeys, the Nile goose, and dogs, since the Old Kingdom period. But once cats were finally domesticated, their popularity was enormous. Gradually, the cat became one of the most universally worshiped animals.

As has been noted, the primary bond distinguishing a pet-and-owner relationship is affection. As useful as many of these animals are, what differentiates a pet from other economically useful livestock is the degree of contact between the animals and human beings. Often, this relationship has been unabashedly sentimentalized in myth, art, and literature. The affection between Alexander the Great and his favourite horse, Bucephalus, has become legendary, while in the modern age the popularity of such canine motion-picture stars as Rin Tin Tin and Lassie is further evidence of the importance placed on the relationship between owner and pet.

The pet-and-owner relationship, however, is not only founded on companionship; since the earliest period of domestication, pets have fulfilled practical, economic ends. Catching other animals to feed their human masters is one of the most fundamental uses of pets, and not only dogs have served in this capacity but cats, hyenas, and lions have also been used for hunting. The aristocratic, rather arcane sport of falconry made use of the natural talent of hawks to aid in hunting game birds. Pets have also been used for the purpose of guardingeither other livestock, the home or territory of their owners, or the owners themselves. Any pet that has a sharp sense of smell or hearing and that makes a loud noise when aroused can be used as a guard, although dogs are the best-known examples. It is thought that the Nile goose, a favourite household pet of the ancient Egyptians, may have served such a purpose. The herding and guarding of livestock is another practical use of pets, in particular the dog. Over the centuries, many specialized breeds of dog have been developed to suit this purpose.

Often, pets have been used as a source of food when other sources become scarce. This has been the case with dogs throughout their history of domestication in both the Old World and the New World. Guinea pigs, domesticated as pets in the New World, also assured a stable food supply.

Pets have also been used to eliminate animal pests. The rat-catching ability of cats is celebrated in fairy tales such as Puss n Boots and Dick Whittington, as is the snake-catching talent of the mongoose in Rudyard Kiplings Rikki-tikki-tavi.

Finally, pets themselves have become a self-perpetuating industry, bred for a variety of purposes, including their value as breeding animals. Pets that are bred for aesthetic purposes may have full-fledged show careers. Other pets may be bred for racing or other competitive sports, around which sizable industries have been built.

Animals kept as pets can be classified according to the type of premises or habitat they usually occupy. Dogs, cats, and birds such as canaries and parakeets are kept as household pets. Other birds, such as jays, magpies, and members of the crow family, are kept in aviaries. When kept as pets, reptiles and amphibians frequently require special conditions of heat and moisture. For this reason, they are best kept in glassed enclosures called vivaria. The most common vivarium pets are snakes, lizards, turtles, frogs, and toads. Many people keep fish as aquarium pets. Fishes constitute a completely separate section of the pet world, and an international industry exists for catching, breeding, transporting, and supplying stock. Hutch, or cage, pets can be kept indoors or outdoors under protected conditions. These pets include rabbits, guinea pigs, rats, mice, hamsters, gerbils, and, recently, chinchillas. Paddock pets are those that must be stabled outdoors and include such animals as horses, ponies, donkeys, and mules. Several kinds of insects are also kept as pets. These include walking-stick insects (kept in simple containers at room temperature) and ants (kept in artificial nests).

Of increasing concern is the sale of exotic pets (e.g., jaguars, alligators, ocelots, monkeys, apes, kinkajous, etc.). Rarely are the owners of such pets able to provide the basic nutritional or habitat needs of these animals; most of the animals soon die or are sent to a zoo. Furthermore, in order to obtain the young, which are considered most desirable as pets, many adults of the wild species are killed, seriously depleting populations already endangered. Several countries have passed laws to prohibit the importation of endangered species as pets, but an active black market flourishes.

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Pet | Definition, Types, History, & Facts | Britannica

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2016 psychological thriller film directed by Carles Torrens

Pet is a 2016 psychological thriller film directed by Carles Torrens, written by Jeremy Slater, and starring Dominic Monaghan, Ksenia Solo, Jennette McCurdy, and Nathan Parsons.[4][5][6] The film premiered at South by Southwest on March 11, 2016 [7][8] and was released to theaters on December 2, 2016 by Orion Pictures and Samuel Goldwyn Films.

Seth is a severely introverted man who works at an animal control center. He has developed an obsession with Holly, a waitress and former high school classmate of his, after he saw her writing in her journal on the bus. Seth seeks advice from security guard Nate, who tells him to be confident and approach her. Seth extensively researches Holly's online profiles and tries to ask her out, but she rebuffs him. At home, Holly tells her friend Claire about Seth, and takes a drunken phone call from her ex-boyfriend Eric.

Holly receives a bouquet at work the next day, and, assuming they are from Eric, goes to the bar where he works. Seth, who has been following her, confronts her, leading to a physical confrontation when he refuses to accept her rejection. Eric attacks Seth, but Seth is able to steal Holly's journal, which he spends the next several days reading. At work, Seth discovers a trapdoor to a room in an abandoned wing of the animal shelter, where he sets about constructing a steel cage. He follows Holly home, breaks into her apartment, and kidnaps her.

After awakening in the cage, Holly vows to survive, speaking to an image of Claire. Seth informs Holly that he loves her and has imprisoned her to "save" her. Through reading Holly's journal, Seth has learned that Eric slept with Claire, which Holly confronted the latter about during a car ride. In her anger, Holly continued accelerating the car until they were hit by a truck. Although injured, Claire had survived, but Holly fatally stabbed her with a glass shard; Claire's death was attributed to the crash. Since then, Holly has committed a series of gruesome murders and written about them in her journal, leading to Seth finding a "purpose" in life by preventing Holly from hurting anyone else.

Over the next several days, they engage in psychological mind games against each other as Holly begins to slip details to draw Seth in. Seth maintains that Holly committed the other murders out of guilt for not being caught over Claire, but Holly counters that she kills simply for pleasure. A suspicious Nate follows Seth and discovers Holly. She deliberately distracts Nate so that Seth has time to overpower him. At Holly's urging, he smashes Nate's skull with a cinder block, then follows her instructions to dispose of the body.

The police become suspicious of Seth's role in Nate's disappearance. Holly convinces him that he can save her if he proves his love to her by cutting off his finger. He does, but this leads to Holly grabbing his knife and threatening to kill herself if he doesn't release her. She says she finally believes that he loves her before slitting his throat.

Some time later, Holly is back together with Eric, and the "fictional" events from her journal are being published by a vanity press. Holly finds evidence that Eric has been cheating again, but declines to hurt him. Instead, she travels to a warehouse, where it is revealed that Seth is being kept in a cage, still alive but horribly mutilated and tortured; she thanks him for "saving" her by allowing her to take out all of her murderous impulses on him instead.

It was announced in August 2015 that filming had begun with actors Dominic Monaghan, Ksenia Solo, Jennette McCurdy, and Nathan Parsons.[4][5][6]

The film premiered at the March 2016 South by Southwest Film festival.[7][8][9]

Pet was released to nine theatres on December 2, 2016 with total gross of $8,004.[10][11] It was set for a June 16, 2017 theatrical opening in Spain.[12]

Reviews for Pet have been mixed, with critics alternatively praising the subversive themes and strong leading performances, or lamenting the implausible twists. The review aggregator website Rotten Tomatoes reported that 56% of critics have given the film a positive review based on 18 reviews, with an average rating of 5.16/10.[13] On Metacritic, the film has a weighted average score of 48 out of 100 based on 8 critics, indicating "mixed or average reviews".[14] Reviews that have criticized the twists include Screen Anarchy, which wrote "Without spoiling anything more, the twists push past the merely unlikely into a strange minefield of 'what in the world?'",[15] and RogerEbert.com, which noted "The rank, idiotic implausibilities continue to mount..."[16]

The Hollywood Reporter gave the bottom line of "This graphically violent horror thriller features too many plot twists for its own good", but the review has also words of praise for the direction and cast: "Still, the film is engrossing, thanks to the directors skill at delivering sustained tension, and the excellent performances."[17]

An entirely positive review came from The A.V. Club's Alex McCown, who stated: "Part of the wicked fun of Pet, a dark little exercise in sadism and black humor, is how it upends the traditional conventions of the 'wronged woman turns the tables on her abuser' narrative. (...) The films zigs where you expect a depraved zag, resulting in a smart and unsettling tale."[18]

Another overall positive review has been given by Katie Walsh of Los Angeles Times, who wrote: "The constant power flipping allows for some interesting explorations of both the misogyny and misandry demonstrated by the main characters, and the way they justify their actions through the philosophical lens of love and sacrifice. 'Pet' is a modern-day fable of unchecked desire that descends quickly into a bloody, morbid cautionary tale."[19]

Francisco Marinero of El Mundo rated Pet 2 out 5 stars, writing that the film, which as usual in American independent pictures stars a "nondescript guy sadly alone in domestic routines", "is conceived as a function of the bombshells in its writing and characters", favouring gruesomeness over suspense.[20]

Link:
Pet (film) - Wikipedia

OverviewWhat is DiabetesWhat is diabetes?

Diabetes happens when your body isn't able to take up sugar (glucose) into its cells and use it for energy. This results in a build up of extra sugar in your bloodstream.

Mismanagement of diabetes can lead to serious consequences, causing damage to a wide range of your body's organs and tissues including your heart, kidneys, eyes and nerves.

The process of digestion includes breaking down the food you eat into various different nutrient sources. When you eat carbohydrates (for example, bread, rice, pasta), your body breaks this down into sugar (glucose). When glucose is in your bloodstream, it needs help a "key" to get into its final destination where it's used, which is inside your body's cells (cells make up your body's tissues and organs). This help or "key" is insulin.

Insulin is a hormone made by your pancreas, an organ located behind your stomach. Your pancreas releases insulin into your bloodstream. Insulin acts as the key that unlocks the cell wall door, which allows glucose to enter your bodys cells. Glucose provides the fuel or energy tissues and organs need to properly function.

If you have diabetes:

Or

If glucose cant get into your bodys cells, it stays in your bloodstream and your blood glucose level rises.

The types of diabetes are:

Less common types of diabetes include:

Diabetes insipidus is a distinct rare condition that causes your kidneys to produce a large amount of urine.

Some 34.2 million people of all ages about 1 in 10 have diabetes in the U.S. Some 7.3 million adults aged 18 and older (about 1 in 5) are unaware that they have diabetes (just under 3% of all U.S. adults). The number of people who are diagnosed with diabetes increases with age. More than 26% of adults age 65 and older (about 1 in 4) have diabetes.

Factors that increase your risk differ depending on the type of diabetes you ultimately develop.

Risk factors for Type 1 diabetes include:

Risk factors for prediabetes and Type 2 diabetes include:

Risk factors for gestational diabetes include:

The cause of diabetes, regardless of the type, is having too much glucose circulating in your bloodstream. However, the reason why your blood glucose levels are high differs depending on the type of diabetes.

Symptoms of diabetes include:

Other symptoms

Type 1 diabetes symptoms: Symptoms can develop quickly over a few weeks or months. Symptoms begin when youre young as a child, teen or young adult. Additional symptoms include nausea, vomiting or stomach pains and yeast infections or urinary tract infections.

Type 2 diabetes and prediabetes symptoms: You may not have any symptoms at all or may not notice them since they develop slowly over several years. Symptoms usually begin to develop when youre an adult, but prediabetes and Type 2 diabetes is on the rise in all age groups.

Gestational diabetes: You typically will not notice symptoms. Your obstetrician will test you for gestational diabetes between 24 and 28 weeks of your pregnancy.

If your blood glucose level remains high over a long period of time, your bodys tissues and organs can be seriously damaged. Some complications can be life-threatening over time.

Complications include:

Complications of gestational diabetes:

In the mother: Preeclampsia (high blood pressure, excess protein in urine, leg/feet swelling), risk of gestational diabetes during future pregnancies and risk of diabetes later in life.

In the newborn: Higher-than-normal birth weight, low blood sugar (hypoglycemia), higher risk of developing Type 2 diabetes over time and death shortly after birth.

Diabetes is diagnosed and managed by checking your glucose level in a blood test. There are three tests that can measure your blood glucose level: fasting glucose test, random glucose test and A1c test.

Less than 100

Less than 140

Less than 5.7%

Gestational diabetes tests: There are two blood glucose tests if you are pregnant. With a glucose challenge test, you drink a sugary liquid and your glucose level is checked one hour later. You dont need to fast before this test. If this test shows a higher than normal level of glucose (over 140 ml/dL), an oral glucose tolerance test will follow (as described above).

Type 1 diabetes: If your healthcare provider suspects Type 1 diabetes, blood and urine samples will be collected and tested. The blood is checked for autoantibodies (an autoimmune sign that your body is attacking itself). The urine is checked for the presence of ketones (a sign your body is burning fat as its energy supply). These signs indicate Type 1 diabetes.

If you have symptoms or risk factors for diabetes, you should get tested. The earlier diabetes is found, the earlier management can begin and complications can be lessened or prevented. If a blood test determines you have prediabetes, you and your healthcare professional can work together to make lifestyle changes (e.g. weight loss, exercise, healthy diet) to prevent or delay developing Type 2 diabetes.

Additional specific testing advice based on risk factors:

Diabetes affects your whole body. To best manage diabetes, youll need to take steps to manage your risk factors, including:

You hold the keys to managing your diabetes by:

Checking your blood glucose level is important because the results help guide decisions about what to eat, your physical activity and any needed medication and insulin adjustments or additions.

The most common way to check your blood glucose level is with a blood glucose meter. With this test, you prick the side of your finger, apply the drop of blood to a test strip, insert the strip into the meter and the meter will show your glucose level at that moment in time. Your healthcare provider will tell you how often youll need to check your glucose level.

Advancements in technology have given us another way to monitor glucose levels. Continuous glucose monitoring uses a tiny sensor inserted under your skin. You don't need to prick your finger. Instead, the sensor measures your glucose and can display results anytime during the day or night. Ask your healthcare provider about continuous glucose monitors to see if this is an option for you.

Ask your healthcare team what your blood glucose level should be. They may have a specific target range for you. In general, though, most people try to keep their blood glucose levels at these targets:

Having a blood glucose level that is lower than the normal range (usually below 70 mg/dL) is called hypoglycemia. This is a sign that your body gives out that you need sugar.

Symptoms you might experience if you have hypoglycemia include:

You might pass out if your hypoglycemia is not managed.

If you have too much glucose in your blood, you have a condition called hyperglycemia. Hyperglycemia is defined as:

or

Treatments for diabetes depend on your type of diabetes, how well managed your blood glucose level is and your other existing health conditions.

Oral medications and insulin work in one of these ways to treat your diabetes:

Over 40 medications have been approved by the Food and Drug Administration for the treatment of diabetes. Its beyond the scope of this article to review all of these drugs. Instead, well briefly review the main drug classes available, how they work and present the names of a few drugs in each class. Your healthcare team will decide if medication is right for you. If so, theyll decide which specific drug(s) are best to treat your diabetes.

Diabetes medication drug classes include:

Many oral diabetes medications may be used in combination or with insulin to achieve the best blood glucose management. Some of the above medications are available as a combination of two medicines in a single pill. Others are available as injectable medications, for example, the GLP-1 agonist semaglutide (Ozempic) and lixisenatide (Adlyxin).

Always take your medicine exactly as your healthcare prescribes it. Discuss your specific questions and concerns with them.

There are many types of insulins for diabetes. If you need insulin, you healthcare team will discuss the different types and if they are to be combined with oral medications. To follow is a brief review of insulin types.

There are insulins that are a combination of different insulins. There are also insulins that are combined with a GLP-1 receptor agonist medication (e.g. Xultophy, Soliqua).

Insulin is available in several different formats. You and your healthcare provider will decide which delivery method is right for you based on your preference, lifestyle, insulin needs and insurance plan. Heres a quick review of available types.

Yes. There are two types of transplantations that might be an option for a select number of patients who have Type 1 diabetes. A pancreas transplant is possible. However, getting an organ transplant requires taking immune-suppressing drugs for the rest of your life and dealing with the side effects of these drugs. However, if the transplant is successful, youll likely be able to stop taking insulin.

Another type of transplant is a pancreatic islet transplant. In this transplant, clusters of islet cells (the cells that make insulin) are transplanted from an organ donor into your pancreas to replace those that have been destroyed.

Another treatment under research for Type 1 diabetes is immunotherapy. Since Type 1 is an immune system disease, immunotherapy holds promise as a way to use medication to turn off the parts of the immune system that cause Type 1 disease.

Bariatric surgery is another treatment option thats an indirect treatment for diabetes. Bariatric surgery is an option if you have Type 2 diabetes, have obesity (body mass index over 35) and considered a good candidate for this type of surgery. Much improved blood glucose levels are seen in people who have lost a significant amount of weight.

Of course other medications are prescribed to treat any existing health problems that contribute to increasing your risk of developing diabetes. These conditions include high blood pressure, high cholesterol and other heart-related diseases.

Although diabetes risk factors like family history and race cant be changed, there are other risk factors that you do have some control over. Adopting some of the healthy lifestyle habits listed below can improve these modifiable risk factors and help to decrease your chances of getting diabetes:

No. Type 1 diabetes is an autoimmune disease, meaning your body attacks itself. Scientists arent sure why someones body would attack itself. Other factors may be involved too, such as genetic changes.

Chronic complications are responsible for most illness and death associated with diabetes. Chronic complications usually appear after several years of elevated blood sugars (hyperglycemia). Since patients with Type 2 diabetes may have elevated blood sugars for several years before being diagnosed, these patients may have signs of complications at the time of diagnosis.

The complications of diabetes have been described earlier in this article. Although the complications can be wide ranging and affect many organ systems, there are many basic principles of prevention that are shared in common. These include:

If you have diabetes, the most important thing you can do is keep your blood glucose level within the target range recommended by your healthcare provider. In general, these targets are:

You will need to closely follow a treatment plan, which will likely include following a customized diet plan, exercising 30 minutes five times a week, quitting smoking, limiting alcohol and getting seven to nine hours of sleep a night. Always take your medications and insulin as instructed by your provider.

If you havent been diagnosed with diabetes, you should see your healthcare provider if you have any symptoms of diabetes. If you already have been diagnosed with diabetes, you should contact your provider if your blood glucose levels are outside of your target range, if current symptoms worsen or if you develop any new symptoms.

Sugar itself doesn't directly cause diabetes. Eating foods high in sugar content can lead to weight gain, which is a risk factor for developing diabetes. Eating more sugar than recommended American Heart Association recommends no more than six teaspoons a day (25 grams) for women and nine teaspoons (36 grams) for men leads to all kinds of health harms in addition to weight gain.

These health harms are all risk factors for the development of diabetes or can worsen complications. Weight gain can:

Most people with diabetes see their primary healthcare provider first. Your provider might refer you to an endocrinologist/pediatric endocrinologist, a physician who specializes in diabetes care. Other members of your healthcare team may include an ophthalmologist (eye doctor), nephrologist (kidney doctor), cardiologist (heart doctor), podiatrist (foot doctor), neurologist (nerve and brain doctor), gastroenterologist (digestive tract doctor), registered dietician, nurse practitioners/physician assistants, diabetes educator, pharmacist, personal trainer, social worker, mental health professional, transplant team and others.

In general, if you are being treated with insulin shots, you should see your doctor at least every three to four months. If you are treated with pills or are managing diabetes through diet, you should be seen at least every four to six months. More frequent visits may be needed if your blood sugar isn't managed or if complications of diabetes are worsening.

Although these seem like simple questions, the answers are not so simple. Depending on the type of your diabetes and its specific cause, it may or may not be possible to reverse your diabetes. Successfully reversing diabetes is more commonly called achieving remission.

Type 1 diabetes is an immune system disease with some genetic component. This type of diabetes cant be reversed with traditional treatments. You need lifelong insulin to survive. Providing insulin through an artificial pancreas (insulin pump plus continuous glucose monitor and computer program) is the most advanced way of keeping glucose within a tight range at all times most closely mimicking the body. The closest thing toward a cure for Type 1 is a pancreas transplant or a pancreas islet transplant. Transplant candidates must meet strict criteria to be eligible. Its not an option for everyone and it requires taking immunosuppressant medications for life and dealing with the side effects of these drugs.

Its possible to reverse prediabetes and Type 2 diabetes with a lot of effort and motivation. Youd have to reverse all your risk factors for disease. To do this means a combination of losing weight, exercising regularly and eating healthy (for example, a plant-based, low carb, low sugar, healthy fat diet). These efforts should also lower your cholesterol numbers and blood pressure to within their normal range. Bariatric surgery (surgery that makes your stomach smaller) has been shown to achieve remission in some people with Type 2 diabetes. This is a significant surgery that has its own risks and complications.

If you have gestational diabetes, this type of diabetes ends with the birth of your child. However, having gestational diabetes is a risk factor for developing Type 2 diabetes.

The good news is that diabetes can be effectively managed. The extent to which your Type 1 or Type 2 diabetes can be managed is a discussion to have with your healthcare provider.

Yes, its possible that if diabetes remains undiagnosed and unmanaged (severely high or severely low glucose levels) it can cause devastating harm to your body. Diabetes can cause heart attack, heart failure, stroke, kidney failure and coma. These complications can lead to your death. Cardiovascular disease in particular is the leading cause of death in adults with diabetes.

Although having diabetes may not necessarily increase your risk of contracting COVID-19, if you do get the virus, you are more likely to have more severe complications. If you contract COVID-19, your blood sugars are likely to increase as your body is working to clear the infection. If you contract COVID-19, contact your healthcare team early to let them know.

Blood vessels are located throughout our bodys tissues and organs. They surround our bodys cells, providing a transfer of oxygen, nutrients and other substances, using blood as the exchange vehicle. In simple terms, diabetes doesnt allow glucose (the bodys fuel) to get into cells and it damages blood vessels in/near these organs and those that nourish nerves. If organs, nerves and tissues cant get the essentials they need to properly function, they can begin to fail. Proper function means that your hearts blood vessels, including arteries, are not damaged (narrowed or blocked). In your kidneys, this means that waste products can be filtered out of your blood. In your eyes, this means that the blood vessels in your retina (area of your eye that provides your vision) remain intact. In your feet and nerves, this means that nerves are nourished and that theres blood flow to your feet. Diabetes causes damage that prevents proper function.

Unmanaged diabetes can lead to poor blood flow (poor circulation). Without oxygen and nutrients (delivered in blood), you are more prone to the development of cuts and sores that can lead to infections that cant fully heal. Areas of your body that are farthest away from your heart (the blood pump) are more likely to experience the effects of poor blood flow. So areas of your body like your toes, feet, legs and fingers are more likely to be amputated if an infection develops and healing is poor.

Yes. Because unmanaged diabetes can damage the blood vessels of the retina, blindness is possible. If you havent been diagnosed with diabetes yet but are experiencing a change in your vision, see primary healthcare provider or ophthalmologist as soon as you can.

Scientists dont have firm answers yet but there appears to be a correlation between hearing loss and diabetes. According to the American Diabetes Association, a recent study found that hearing loss was twice as common in people with diabetes versus those who didnt have diabetes. Also, the rate of hearing loss in people with prediabetes was 30% higher compared with those who had normal blood glucose levels. Scientists think diabetes damages the blood vessels in the inner ear, but more research is needed.

Yes, its possible to develop headaches or dizziness if your blood glucose level is too low usually below 70 mg/dL. This condition is called hypoglycemia. You can read about the other symptoms hypoglycemia causes in this article. Hypoglycemia is common in people with Type 1 diabetes and can happen in some people with Type 2 diabetes who take insulin (insulin helps glucose move out of the blood and into your bodys cells) or medications such as sulfonylureas.

Yes, its possible for diabetes to cause hair loss. Unmanaged diabetes can lead to persistently high blood glucose levels. This, in turn, leads to blood vessel damage and restricted flow, and oxygen and nutrients cant get to the cells that need it including hair follicles. Stress can cause hormone level changes that affect hair growth. If you have Type 1 diabetes, your immune system attacks itself and can also cause a hair loss condition called alopecia areata.

People with Type 1 diabetes need insulin to live. If you have Type 1 diabetes, your body has attacked your pancreas, destroying the cells that make insulin. If you have Type 2 diabetes, your pancreas makes insulin, but it doesnt work as it should. In some people with Type 2 diabetes, insulin may be needed to help glucose move from your bloodstream to your bodys cells where its needed for energy. You may or may not need insulin if you have gestational diabetes. If you are pregnant or have Type 2 diabetes, your healthcare provider will check your blood glucose level, assess other risk factors and determine a treatment approach which may include a combination of lifestyle changes, oral medications and insulin. Each person is unique and so is your treatment plan.

You arent born with diabetes, but Type 1 diabetes usually appears in childhood. Prediabetes and diabetes develop slowly over time. Gestational diabetes occurs during pregnancy. Scientists do believe that genetics may play a role or contribute to the development of Type 1 diabetes. Something in the environment or a virus may trigger its development. If you have a family history of Type 1 diabetes, you are at higher risk of developing Type 1 diabetes. If you have a family history of prediabetes, Type 2 diabetes or gestational diabetes, youre at increased risk of developing prediabetes, Type 2 diabetes or gestational diabetes.

Diabetes-related ketoacidosis is a life-threatening condition. It happens when your liver breaks down fat to use as energy because theres not enough insulin and therefore glucose isnt being used as an energy source. Fat is broken down by the liver into a fuel called ketones. The formation and use of ketones is a normal process if it has been a long time since your last meal and your body needs fuel. Ketones are a problem when your fat is broken down too fast for your body to process and they build up in your blood. This makes your blood acidic, which is a condition called ketoacidosis. Diabetes-related ketoacidosis can be the result of unmanaged Type 1 diabetes and less commonly, Type 2 diabetes. Diabetes-related ketoacidosis is diagnosed by the presence of ketones in your urine or blood and a basic metabolic panel. The condition develops over several hours and can cause coma and possibly even death.

Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) develops more slowly (over days to weeks) than diabetes-related ketoacidosis. It occurs in patients with Type 2 diabetes, especially the elderly and usually occurs when patients are ill or stressed. If you have HHNS, you blood glucose level is typically greater than 600 mg/dL. Symptoms include frequent urination, drowsiness, lack of energy and dehydration. HHNS is not associated with ketones in the blood. It can cause coma or death. Youll need to be treated in the hospital.

This means your kidneys are allowing protein to be filtered through and now appear in your urine. This condition is called proteinuria. The continued presence of protein in your urine is a sign of kidney damage.

A note from Cleveland Clinic

Theres much you can do to prevent the development of diabetes (except Type 1 diabetes). However, if you or your child or adolescent develop symptoms of diabetes, see your healthcare provider. The earlier diabetes is diagnosed, the sooner steps can be taken to treat and manage it. The better you are able to manage your blood sugar level, the more likely you are to live a long, healthy life.

Originally posted here:
Diabetes: An Overview - Cleveland Clinic

The use of stem cell therapy in treating patients with autism spectrum disorder (ASD) is not recommended and its promotion and advertisement will be considered professional misconduct, the National Medical Commission (NMC) has said.

The NMCs ethics and medical registration board set up a committee to look into the prescription, recommendation, or administration of such treatment after doctors and parents complained about the mushrooming stem cell therapy centres and their advertisements promising cure for autism. The committee submitted its report on December 6 and it was uploaded on December 14.

The medical fraternity has welcomed the order, saying, there is not scientific basis to this line of treatment for which patients have been shelling out for years.

Dr Samir Dalwai, developmental-behavioural paediatrician, Nanavati Max Hospital, Vile Parle, said, Autism is a chronic condition and the results are slow. And there is a stigma attached to it. However, desperate parents fall for such promotional gimmicks as the therapy is marketed well not just in the city but across the country.

Every week, the hospital gets at least one patient in the 7-8 age group whose parents have tried stem cell therapy to treat autism, but in vain. Because of the stigma or being told by doctors that there wont be much, or slow improvement in their child, parents fall for the stem cell advertisements. Many a time, patients stopped the treatment midway and opted for the therapy hoping to see the miracle cure it promises, he said, adding each therapy reportedly costs 3- 4 lakh.

The neuro-developmental paediatric chapter of Indian Academy of Paediatrics had also written to all government authorities to take action in this regard.

Parul Kumtha, trustee, Forum for Autism, said the therapy neither had enough proof of efficacy nor did it have the Food and Drug Administrations approval.

Many parents have mortgaged their jewellery, property to bear the cost of treatment. If any medical centres are doing research on stem cell therapy, then they should not charge the patients. Also, as the NMC order says, there is no cure for autism and it is medically unethical to promise it as a cure, she said.

Dr Milan Balakrishnan, psychiatrist and member of Bombay Psychiatric Society, said it has been observed that after the therapy, there is a rise in irritability and aggression in the patient.

Recently, a 15-year-old boy with autism was brought to us. He had a lot of anger, and he was beating up his parents too. We had to manage the outbursts with medication. It was during the course of treatment that the parents told us about stem cell therapy and the aggression their son developed as a new symptom after the procedure, he said.

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Banking

The Federal Reserve just raised rates. Heres what it could mean for inflation and interest rates in the new year.

5 min read

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Live Cell Imaging Market accounted for US$ 1.8 billion in 2022 and is estimated to be US$ 5.0 billion by 2032 and is anticipated to register a CAGR of 9.2% - By PMI  India Shorts

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Live Cell Imaging Market accounted for US$ 1.8 billion in 2022 and is estimated to be US$ 5.0 billion by 2032 and is anticipated to register a CAGR of...