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Human induced pluripotent stem cells (hipscs) may provide potential resource for regenerative medicine research, including generation of insulin-producing cells for diabetes research and insulin production. Testosterone (t) is an androgen hormone which promotes protein synthesis and improves the management of type 2 diabetes in clinical studies. Concurrently, co-existed hyperandrogenism and hyperinsulinism is frequently observed in polycystic ovary syndrome, congenital adrenal hyperplasia and some of wermer's syndrome. However, the relationship among androgens, insulin and the differentiation of pancreatic β cells is still not fully clear. Here we find that t improves the differentiation efficiency of insulin-producing cells from hipscs. The addition of t into routine differentiation formula for pancreatic β cells increases the differentiation efficiency from 12% to 35%. The administration of t promotes the expression of key genes associated with β cells differentiation including ngn3, neurod1 and ins. This finding benefits the ongoing process to optimize the differentiation protocol of pancreatic β cells from hipscs, and provides some degree of understanding the clinical management of t for type 2 diabetes.type diabetes
Diabetic nephropathy refers to diabetic kidney disease (nehpro=kidneys, pathy=disease). In 2011, diabetes caused nearly 44% of kidney failure cases. This makes diabetic kidney disease the number one complication of diabetes; one that is likely to affect almost every diabetic to some extent. In nearly half the cases of kidney disease, it could lead to kidney failure as well.
Diabetes and kidneys:
The kidneys filter nearly 200 quarts of our blood every day. Diabetes is a disease of excess sugar in our blood. Read these two sentences together and the link between diabetes and kidneys becomes obvious!
Every single day of our lives, the kidneys perform these functions:
Remove waste from our body (in the form of urine) retain whatever proteins, vitamins and other nutrients we can still usebalance the fluids in the bodyhelp maintain proper blood pressure by managing potassium and calcium levelskeep bones healthyhelp make red blood cells.
Diabetes damages the kidneys and the urinary system in three main ways:
Damage to blood vessels in the kidneys: too much sugar damages the filters in the kidneysdamage to nerves: fine nerves in the hands, feet, etc. Are corroded by the extra sugar in the blooddamage to the urinary tract: nerves run from our bladder to our brain and let us know when the bladder is full and we need to go. Damage to these nerves could mean we don’t react when our bladder is full. Result: extra pressure on the kidneys. Retained urine can also allow urinary tract infections to grow and migrate back to the kidneys.
Diabetes damage to blood vessels inside kidneys: The filtering units of the kidneys are called glomerules. They have tiny blood vessels that are easily clogged and damaged by excess sugar in our blood. Damage to these vessels also causes albumin, a kind of protein to leak via the urine. Ideally, albumin should be retained in the body. It is a condition called microalbuminuria in the early stages and albuminuria in the later stages.
Diabetes damage to nerves: Diabetes can also damage nerves everywhere in the body, a condition that is called diabetic neuropathy. When this happens in our hands and feet, we lose sensation there or begin to feel ‘pins and needles’. Nerves also convey messages from the brain to the urinary bladder and back. They inform the brain when our bladder is full. However, when these nerves are damaged by excess blood sugar, the brain does not realize when the bladder is full. The pressure from a full bladder can damage our kidneys over time.
Diabetes damage to urinary tract damage: When urine is retained in the bladder for long, the risk of bacterial infections increases. Bacteria also thrive on sugar, so diabetes increases infection risk. These infections usually stay limited to the urinary bladder. However, if they last for long, they may migrate to the kidneys and damage them too.
Consider all this in an organ that is working 24×7. Now you see why diabetic kidney failure is such a real danger for diabetics over the long term.
Diabetic kidney failure: early stages and symptoms
Diabetic kidney failure is a very real threat. It is a slow but relentless process that is divided into five stages of deterioration. The last stage called diabetic kidney failure or end stage renal disease (esrd)
The 5 stages leading to diabetic kidney failure are:
Stage 1: Kidney damage with normal gfr (90 or more). Gfr or glomuler filtration rate is the most widely accepted measure of kidney function. There are often no symptoms at this stage.
Stage 2: Kidney damage with mild decrease in gfr (60 to 89). Again, most patients feel no specific symptoms till this point.
Stage 3: Moderate decrease in gfr (30 to 59). At this stage, you may be losing too much protein, calcium and other nutrients. Some patients may feel breathless (due to loss of iron and anemia). Some puffiness and water retention could also be visible in the body. Urine may turn brown in colour. Some patients feel back pain too.
Stage 4: Severe reduction in gfr (15 to 29). All of the symptoms of stage 3 will are felt even more acutely now. Some blood may be seen in the urine. Breathlessness and swelling are usually quite severe. The stage at which you will need to finalize dialysis or kidney transplant options
Stage 5: Kidney failure (gfr less than 15). The kidneys give up at this stage. You will need dialysis or a kidney transplant.
Symptoms of kidney disease in diabetic patients
• Frequent urination, especially at night
• Blood or other dark discharge in the urine
• Swelling in the ankles
• Cramps in the calf muscles of the legs
• Feeling sick, feeling like throwing up, first thing in the morning
• Feeling weak, tired, breathless, looking pale
• Unexplained and consistent high blood pressure
• Unexplained urge to itch
• Lab tests: protein or albumin in the urine
• Lab tests: higher than normal levels of creatinine or bun in the blood
Diabetes and kidneys: how to protect yourself
First, you doctor needs to be sure that the underlying diabetes is the main cause of the kidney damage. Once this is done, the standard approach is to keep the kidneys working well for as long as possible. You doctor will likely add the hypertension-reducing medications called angiotensin converting enzyme (ace) inhibitors to your regimen. This is because ace inhibitors have been shown to help slow the loss of kidney function.
Here’s what diabetics can do to protect themselves from kidney damage:
• Control your blood sugar better. Don’t rely only on medications, but make changes to diet and lifestyle too. Many doctors endorse intermittent fasting to reverse diabetes today.
• Control high blood pressure. Take prescribed medicines on time. Daily moderate exercise and stress management techniques like meditation can help too.
• Watch out for and get timely treatment for urinary tract infections
• Don’t take medications like over-the-counter pain medications without telling your doctor. These may damage the kidneys, especially if you’re already at risk.
• Watch out for and take steps to prevent diabetic neuropathy. Damaged urinary tract nerves can lead to urinary retention and kidney damage. Some drugs like& metformin can contribute to diabetic nerve damage and supplements like vitamin b12 (as part of a good vitamin b complex) and alpha lipoic acid can help prevent this. Be aware and act soon.
• For people with diabetes, kidney screening once a year is mandatory. This can help to detect any protein or other substances that shouldn’t normally be in the urine.
• Use the right dietary supplements to protect your kidneys from diabetes damage.
Diabetic nephropathy: dietary supplements that help
Vitamin c (200mg- 1250mg per day)
Vitamin c is known to reduce excretion of urinary albumin. This suggests it may slow progression of diabetic nephropathy.
In a study published in the scientific journal nephron, researchers found that supplementation with vitamin c (also known as ascorbic acid or aa) reduced micro albumin loss in diabetic patients. The researchers concluded that “dietary supplementation of aa in diabetic subjects may have long-term benefits in attenuating the progression of diabetic complications”
Vitamin e (100iu-680iu per day)
Studies have found that vitamin e, when administered along with vitamin c, has the ability to reduce urinary albumin excretion. In the first study, published in the journal diabetes care, one groups was given just vitamin e and vitamin c. A second group received these and also the minerals magnesium and zinc. Both groups showed improved kidney function on lab parameters. In the second study, published in the diabetic medicine journal, type 2 diabetics took 1250mg of vitamin c plus 680 iu of vitamin e daily. In four weeks, their albumin excretion rate or aer was 19% lower compared to the placebo group.
Alpha lipoic acid (600mg per day).
Alpha lipoic acid (ala) is found in spinach, broccoli and potatoes and is a known anti-oxidant. A research study in 2001 set out to see if ala could help patients with diabetic kidney damage. The study group received 600 mg of alpha lipoic acid as a supplement. Another group received no supplement. The first group was able to maintain the same rate of urinary albumin loss, while the control group, saw their albumin loss worsen during the same period. Since alpha lipoic acid helps diabetics fight diabetic nerve damage too, it may well be a useful addition to all diabetics.
Everything we eat, including dietary supplements, has to be processed by the kidneys at some point of time. So do involve your doctor in your choice of dietary supplements if you have diabetic kidney disease.
Just remember: diabetic nephropathy or kidney damage is a result of the underlying diabetes. M. D. S are today saying that type 2 diabetes is reversible, through dietary and lifestyle changes. The better your control over the underlying blood sugar levels, the fewer the complications of diabetes. There are dietary supplements that are proven to help you improve blood sugar control, often without the side effects of prescription medications.type diabetes
Boerhaave first described the spontaneous rupture of the esophagus in 1724. It typically occurs after forceful emesis. Boerhaave syndrome is a transmural perforation of the esophagus to be distinguished from mallory-weiss syndrome, a nontransmural esophageal tear also associated with vomiting. Because it often is associated with emesis, boerhaave syndrome usually is not truly spontaneous. However, the term is useful for distinguishing it from iatrogenic perforation, which accounts for 85-90% of cases of esophageal rupture.
Diagnosis of boerhaave syndrome can be difficult because often no classic symptoms are present and delays in presentation for medical care are common. Approximately one third of all cases of boerhaave syndrome are clinically atypical. Prompt recognition of this potentially lethal condition is vital to ensure appropriate treatment. Mediastinitis, sepsis, and shock frequently are seen late in the course of illness, which further confuses the diagnostic picture.
See can't-miss gastrointestinal diagnoses, a critical images slideshow, to help diagnose the potentially life-threatening conditions that present with gastrointestinal symptoms.
A reported mortality estimate is approximately 35%, making it the most lethal perforation of the gi tract. The best outcomes are associated with early diagnosis and definitive surgical management within 12 hours of rupture. If intervention is delayed longer than 24 hours, the mortality rate (even with surgical intervention) rises to higher than 50% and to nearly 90% after 48 hours. Left untreated, the mortality rate is close to 100%.
Esophageal rupture in boerhaave syndrome is postulated to be the result of a sudden rise in intraluminal esophageal pressure produced during vomiting, as a result of neuromuscular incoordination causing failure of the cricopharyngeus muscle to relax. The syndrome commonly is associated with overindulgence in food and/or alcohol. The most common anatomical location of the tear in boerhaave syndrome is at the left posterolateral wall of the lower third of the esophagus, 2-3 cm proximal to the gastroesophageal junction, along the longitudinal wall of the esophagus. The second most common site of rupture is in the subdiaphragmatic or upper thoracic area. [1, 2]
Although likely underreported, the incidence of boerhaave syndrome is relatively rare. A 1980 review by kish cited 300 cases in the literature worldwide.  a 1986 summary by bladergroen et al described 127 cases.  of these, 114 were diagnosed antemortem; the others were diagnosed at autopsy. Overall, boerhaave syndrome accounts for 15% of all cases of traumatic rupture or perforation of the esophagus.
Race-, sex-, and age-related demographics
Cases have been reported in all races and on virtually every continent, affecting males more commonly than females, with ratios ranging from 2: 1 to 5: 1.
Boerhaave syndrome is seen most frequently among patients aged 50-70 years. Reports suggest that 80% of all patients are middle-aged men. However, this condiction has also been described in neonates and in persons older than 90 years. Although no clear explanation exists for this, the least susceptible age group appears to be children aged 1-17 years.
Prognosis is directly contingent on early recognition and appropriate intervention. Early diagnosis of boerhaave syndrome allows prompt surgical repair. Diagnosis and surgery within 24 hours carry a 75% survival rate. This drops to approximately 50% after a 24-hour delay and approximately 10% after 48 hours.
The mortality rate is high. Esophageal perforation is the most lethal perforation of the gi tract. Survival is contingent largely upon early recognition and appropriate surgical intervention.
Overall, the mortality rate is approximately 30%. Mortality is usually due to subsequent infection, including mediastinitis, pneumonitis, pericarditis, or empyema.
Patients who undergo surgical repair within 24 hours of injury have a 70-75% chance of survival. This falls to 35-50% if surgery is delayed longer than 24 hours and to approximately 10% if delayed longer than 48 hours.
Cases of patients surviving without surgery exist but are rare enough to warrant case reports in the medical literature.
Esophageal rupture may lead to the development of septicemia, pneumomediastinum, mediastinitis, massive pleural effusion, empyema, pneumomediastinum, or subcutaneous emphysema.
If the esophageal rupture extends directly into the pleura, hydropneumothorax is expected. In adults, this occurs more commonly on the left side of the pleura. In neonates, esophageal rupture usually occurs on the right side.
After esophageal rupture, free air enters the mediastinum and also may spread to the adjacent structures, resulting in mediastinal abscess or superimposed secondary infection.
Other complications include acute respiratory distress syndrome, pneumomediastinum, pneumothorax, and hydrothorax.