EDWARD Y. SKOLNIK, M.D.

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A gene-edited pig kidney was transplanted into a brain-dead human and kept functioning for a planned 61-day study using only standard approved anti-rejection drugs. The kidney maintained stable electrolyte balance and eliminated the need for dialysis, but antibody-mediated rejection emerged on day 33 and was reversed with plasma exchange and complement inhibition. The study shows a minimally modified pig kidney can sustain human-equivalent kidney function and identifies pre-existing immune cells reactive to pig tissue as a key obstacle to long-term success.

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Researchers studied how the human immune system reacts to a pig kidney transplant in a brain-dead human. They found that specific immune cells in the blood increased significantly, leading to rejection of the kidney by day 33 after the transplant. This research is important because it helps identify ways to improve the success of pig organ transplants in humans, potentially addressing the shortage of available human organs for transplantation.

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Transplanting pig organs into humans offers a potential solution to the global shortage of donor organs, but immune rejection remains the central barrier. Advances in gene editing have extended pig organ survival in preclinical primate studies, and recent attempts in human decedents and living patients have revealed both antibody-driven and cell-driven rejection as key challenges. This review synthesizes what is known about the immune mechanisms involved and highlights the genetic and therapeutic strategies being developed to overcome them.

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Researchers transplanted a pig kidney-thymus combination into a deceased human and tracked the immune response over 61 days. T cells from the recipient infiltrated the organ and specific clones expanded in blood, tissue, and lymph nodes around rejection events. This reveals that T cell-driven rejection of pig organs in humans closely mirrors what happens with human-to-human transplants, informing how future immunosuppression strategies must be designed.

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This study looked at how low health literacy affects patient experiences in women with benign gynecologic conditions, but found no studies that linked the two. Out of over 18,000 articles reviewed, none provided evidence connecting health literacy with patient-reported outcomes. This finding highlights a lack of research in this area, indicating a need for future studies to better understand how health literacy impacts women's health care.

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This research looks at two less common surgical cuts—Maylard and Cherney—used in gynecological operations. It finds that these cuts offer better access to the pelvis and lead to less pain and better healing after surgery compared to the traditional Pfannenstiel incision. By using these techniques, doctors can improve patient recovery while still effectively reaching the necessary areas in the body.

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A 39-year-old woman experienced bleeding four months after a pregnancy termination. Tests showed she had leftover pregnancy tissue and a rare condition called a uterine arteriovenous malformation (AVM). Finding effective ways to treat both issues is tricky, as they can increase bleeding risks, so the patient focused on treatment options that would save her blood and protect her ability to have children in the future.

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Researchers studied the role of a protein called Discoidin Domain Receptor 1 (DDR1) in polycystic kidney disease (PKD) and found that even though DDR1 was increased in mouse models of the disease, removing it did not slow down cyst growth or help preserve kidney function. This means that DDR1 is not a good target for new drug treatments for PKD. These findings are important because they can save time and resources, preventing others from exploring DDR1 in future research on this condition.

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This study focused on how a process called glutamine metabolism affects cyst growth in a genetic kidney disease known as autosomal-dominant polycystic kidney disease (ADPKD). Researchers found that a specific enzyme, GLS1, was more active in cells lining the cysts in both human and mouse models of this disease. When they used a drug to block GLS1 in mouse models, they observed that it slowed cyst growth in one type of model but had no effect in another, indicating that targeting this enzyme may be a promising strategy for treating ADPKD, though more research is needed to fully understand how it works.

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Researchers studied a protein called PHPT-1 in mice to understand its role in moving potassium channels to the surface of pancreatic cells. They found that mice lacking PHPT-1 had high insulin levels and low blood sugar, similar to a human condition called congenital hyperinsulinism, due to problems with how the potassium channels function. This research is important because it highlights how PHPT-1 is essential for normal insulin regulation, and issues with this protein could explain some unexplained cases of hyperinsulinism in people.

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This study looked at a protein called NDPK-C and its role in how heart cells manage signals in chronic heart failure (HF). Researchers found that higher levels of NDPK-C in heart failure were linked to lower amounts of a molecule called cAMP, which is crucial for heart contractions. By understanding how NDPK-C works, we can see why heart failure leads to weaker heart function, potentially opening the door for new treatments to improve heart health.

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This study looked at how a protein called PLCε1 helps immune cells, specifically T-cells, stick to blood vessels and move toward areas of inflammation. The researchers found that PLCε1 is essential for a chemical signal called SDF-1α to activate a key process that allows T-cells to adhere and migrate; when PLCε1 was disrupted in mice, the T-cells had trouble reaching inflamed skin, although their ability to produce other immune responses remained intact. This is important because targeting PLCε1 might lead to new treatments for conditions where T-cells improperly migrate to inflamed tissues, like in autoimmune diseases.

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Researchers studied a protein called PI3KC2β to see how it affects mast cells, which play a key role in allergic reactions. They discovered that mice lacking this protein showed significantly reduced allergic responses, including less calcium entry and cytokine release in their mast cells. This is important because it suggests that targeting PI3KC2β could lead to new treatments for allergies and related conditions.

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Researchers studied a protein called NDPKB and its role in eye damage related to diabetes using mice. They found that mice lacking NDPKB had increased damage to blood vessels in the retina, showing significant loss of supportive cells and formation of empty spaces where blood vessels should be. This is important because it highlights how NDPKB helps protect the retina, suggesting that understanding this protein could lead to better treatments for diabetic eye diseases.

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This study looked at how to choose the best treatment for small kidney tumors in patients with mild to moderate chronic kidney disease (CKD). It found that using a scoring system to assess tumor anatomy (the nephrometry score) led to a slight increase in life expectancy—about 0.48 years for 65-year-old men and 0.37 years for women—compared to doing surgery without that assessment. This is important because it suggests that personalized treatment approaches can help patients with CKD live longer by reducing kidney damage and related health risks.

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Researchers studied a protein called PGAM5 to understand its role in regulating certain immune cells called CD4(+) T cells. They found that PGAM5 helps turn off a process that activates these T cells by dephosphorylating another protein, NDPK-B, which is necessary for T cell activation. This discovery is important because it opens up new avenues for understanding immune responses and could have implications for treating diseases related to T cell activity.

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Researchers studied a potassium channel in mammals, specifically KCa3.1, to understand how it functions when it encounters copper, which usually inhibits it. They discovered that when a specific part of the channel gets phosphorylated, it prevents copper from blocking the channel, leading to more calcium entering cells and boosting immune responses. This discovery is important because it reveals a new way that potassium channels can be regulated, which may influence how the immune system works.

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This study looked at two different types of Class IV lupus nephritis (LN) to see if they should be treated differently. Researchers analyzed kidney tissue samples from 78 patients and found that the two subtypes—global and segmental—didn't show significant differences in treatment outcomes or survival rates. This is important because it suggests that both types of Class IV LN can be treated the same way until more research provides new information.

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This research looked at how ion channels, which help transport charged particles in immune cells, influence the development and response of the immune system. The study found that these channels play critical roles in controlling immune cell activity and development, which is important for fighting infections and preventing autoimmune diseases. Understanding these processes could lead to new treatments that modify immune responses to improve health.

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Researchers studied how a specific protein, nucleoside diphosphate kinase B (NDPKB), affects the activity of potassium channels in smooth muscle cells of mouse arteries, which play a role in blood vessel growth after injury. They found that when NDPKB is activated, it increases potassium channel activity, contributing to the thickening of artery walls (known as neointima formation) after injury. This is significant because blocking this protein's action could lead to new treatments for diseases like atherosclerosis, potentially reducing harmful artery growth after procedures like angioplasty.

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This study looked at how a protein in the kidneys, called TRPV5, helps manage calcium levels in the body. Researchers found that a specific enzyme, NDPK-B, activates this protein, which helps reabsorb calcium, while another enzyme restricts its activity. When NDPK-B was removed in mice, they excreted more calcium in their urine, showing how important this regulation is for maintaining proper calcium balance.

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This study looked at a process called macropinocytosis, where cells take in liquid and nutrients. Researchers found that specific molecules in the cell membrane need to break down in a particular order for this process to work properly. They discovered that certain proteins are essential for this breakdown—without them, cells struggle to take in necessary substances, which is important for understanding how cells interact with their environment.

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This study looked at how a protein called NDPKB affects the growth of blood vessels, a process known as angiogenesis. Researchers found that when NDPKB was removed in zebrafish and mice, the formation of new blood vessels was significantly reduced—by 80% in mouse models of eye disease compared to normal mice. This matters because understanding how NDPKB works could help develop new treatments for conditions that involve abnormal blood vessel growth, like cancer or eye diseases.

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Researchers studied how the loss of certain genes (FoxO1, FoxO3a, and FoxO4) affects insulin production in mice, connecting this to a type of diabetes similar to maturity-onset diabetes of the young (MODY). They found that mice lacking these genes had trouble using carbohydrates for energy, which led to lower insulin secretion and early diabetes symptoms. This is important because it sheds light on how insulin-producing cells fail in diabetes, potentially paving the way for better treatment strategies.

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Researchers studied how certain proteins affect the activation of immune cells called mast cells, which play a key role in allergic reactions. They found that a protein called PI3KC2β is essential for mast cells to respond to allergens, leading to inflammation and allergic symptoms, while another protein, TRIM27, acts as a brake on this process. Mice without TRIM27 had a higher risk of severe allergic reactions, indicating that targeting PI3KC2β could be a promising new way to treat allergies.

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This study looked at how certain proteins in the membranes of immune cells, called lymphocytes, help control their activity. Researchers found that these proteins are crucial for managing levels of important minerals like calcium, which are necessary for the cells to perform their functions, such as producing signals to fight infections. Understanding how these ion channels work is important because it can lead to better treatments for immune-related diseases.

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Researchers studied a 56-year-old man who had severe kidney issues caused by two different diseases happening at the same time: ANCA-associated glomerulonephritis and membranous nephropathy, both of which were linked to specific antibodies in his blood. They found that treating him with specific medications improved his kidney function and reduced the harmful antibodies. This case highlights the importance of accurately identifying the causes of kidney diseases to provide better treatments and outcomes for patients.

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This research looked at how well a special MRI technique could measure kidney function in patients with liver cirrhosis. The study found that this MRI method was 95% accurate in estimating kidney function compared to a standard test, while traditional methods based on blood tests were only 40-60% accurate. This is important because a more accurate kidney function test can improve patient care without adding much time to the MRI procedure and without using harmful radiation.

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Researchers studied the role of specific proteins, Drosha and Dicer, in kidney cells called podocytes, which are important for filtering blood. They found that removing Drosha from these cells in young mice led to a kidney disease called collapsing glomerulopathy, similar to what happens when Dicer is removed. This finding highlights that maintaining the right levels of micro-RNAs produced by Drosha and Dicer is crucial for kidney health, and understanding these processes could lead to new treatments for kidney diseases.

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This study looked at two medications, cyclosporine and tacrolimus, used in kidney transplant patients in Saudi Arabia to see how well they work over time. The researchers found that both medications had similar outcomes in terms of kidney function and patient survival after one and two years, with rejection rates being nearly the same (about 19% for cyclosporine and 21% for tacrolimus). However, patients taking cyclosporine had higher cholesterol and blood pressure levels than those on tacrolimus, which is important for managing long-term health after a transplant.

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This study looked at how a protein called TRIM27 affects immune cells known as CD4 T cells. Researchers found that TRIM27 reduces the activity of another protein important for CD4 T cell function, which leads to decreased calcium influx and lower production of immune signaling molecules. This is significant because it reveals a new way TRIM27 can limit CD4 T cell activity, potentially impacting immune responses.

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Researchers studied how moderate kidney disease affects the regression of atherosclerosis (the buildup of fat in arteries) in a mouse model. They found that while atherosclerosis decreased by 55% in healthy mice, it actually worsened by 17% in mice with kidney disease. This matters because it shows that kidney disease not only raises the risk of heart issues but also makes it harder to treat existing cardiovascular conditions.

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Researchers studied a specific channel in immune cells called KCa3.1 to understand its role in causing colitis, a form of inflammatory bowel disease. They found that mice lacking this channel were less likely to develop severe colitis, indicating that blocking KCa3.1 can help reduce inflammation. Since existing medications that inhibit this channel are safe for humans, this research could lead to new treatments for conditions like Crohn's disease and ulcerative colitis.

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This study looked at how drinking a lot of water affects urine composition in people with autosomal dominant polycystic kidney disease (ADPKD) compared to healthy individuals. The researchers found that drinking a large amount of water (3 liters) reduced a key substance called cAMP in urine by 35% in ADPKD patients and by 58% in healthy individuals after short-term water intake. This is important because it indicates that increased water consumption might help slow the progression of kidney disease in ADPKD patients, and more research is needed to confirm this potential benefit.

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Researchers studied mice that lacked a specific gene called NDPK-B to understand its role in T cell activation. They found that these mice had normal development but their T cells had serious issues activating, with a significant drop in their ability to produce key signaling molecules for immune response. This is important because it shows that targeting NDPK-B could lead to new treatments for diseases driven by certain immune cells, like autoimmune disorders.

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Researchers studied a protein called PI3K-C2beta and its role in activating a potassium channel, KCa3.1, which is important for the activation of T-cells, a type of immune cell. They found that when the levels of PI3K-C2beta were reduced, the activity of the KCa3.1 channel decreased, leading to weaker T-cell activation. This finding is significant because it highlights a critical step in how T-cells function, which could potentially lead to better understanding and treatment of immune-related diseases.

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This study examined how KCa3.1 potassium channels affect fluid buildup in kidney cysts of patients with autosomal-dominant polycystic kidney disease (ADPKD). The researchers found that blocking these channels reduced fluid secretion and cyst growth in lab tests. This is important because finding new treatments that target KCa3.1 channels could help slow the progression of kidney failure in people with ADPKD.

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Researchers studied how a specific protein, PHPT-1, affects the KCa3.1 channel in CD4 T cells, which are important for the immune response. They found that when PHPT-1 is present in higher amounts, it reduces the activity of the KCa3.1 channel. This reduction leads to less calcium entering the cells and slows down T cell growth after activation. Understanding this mechanism is important because it reveals how certain proteins can control immune cell functions, which could lead to new treatments for diseases where the immune system is overactive or underactive.

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This research studied a potassium channel called KCa3.1, which is important for cell functions in blood and muscle tissues. The researchers found that a specific substance, phosphatidylinositol-3 phosphate (PI(3)P), activates this channel indirectly through a unique part of its structure made up of 14 amino acids. Understanding how KCa3.1 is regulated by PI(3)P is important because it could help us learn more about various cell functions and potential treatments for related diseases.

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Researchers studied how a specific receptor in cells (EphB2) responds to a signal (ephrinB1-Fc) that influences cell behavior. They found 127 proteins that are involved in this signaling process, with 40 proteins showing increased presence after the cells received the signal, while six proteins were less abundant. Understanding these interactions is important because it could provide insights into how cells communicate and behave, which has implications for treating conditions like nerve damage or cancer.

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Researchers studied the role of two proteins, p38 and p38-interacting protein (p38IP), in the development of mouse embryos during a critical stage called gastrulation. They found that these proteins are essential for reducing levels of E-cadherin, which is important for cell movement and development. Mutations in p38IP led to problems with eye development, neural tube closure, and the movement of cells necessary for forming body structures, highlighting how crucial these proteins are for proper embryonic development.

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Researchers studied how a protein called myotubularin-related protein 6 (MTMR6) affects the function of immune cells, specifically CD4 T cells. They found that when MTMR6 is present, it reduces calcium influx into these cells, which is crucial for their activation and proliferation. This matters because understanding how MTMR6 regulates T cell activity could help in developing better strategies for boosting immune responses in diseases like infections and cancer.

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This study focused on a group of proteins called myotubularins (MTMs) and how they interact with a specific potassium channel in the body. Researchers discovered that the protein MTMR6 uniquely inhibits this potassium channel by a specific process, while other MTMs do not. Understanding how MTMR6 works and what parts of it are essential for its function is important because it can help us learn how different MTMs contribute to diseases when they are missing or not working correctly.

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Researchers studied how a specific protein, called nucleoside diphosphate kinase B (NDPK-B), activates a potassium channel (KCa3.1) that is important for the activation of immune cells known as T cells. They found that when NDPK-B adds a chemical tag to KCa3.1, it is essential for the channel to work properly and for the T cells to be activated. This finding is important because it helps us understand the mechanisms behind immune responses, which could lead to better treatments for autoimmune diseases and transplant rejection.

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Researchers studied a protein called MTMR6 and found that it can decrease the activity of a specific potassium channel (KCa3.1). When MTMR6 levels were high, the potassium channel activity dropped significantly, which is important because this channel is involved in controlling cell growth and activity in T cells and certain cancer cells. Understanding how MTMR6 regulates this channel could help address issues related to excessive cell growth in diseases like cancer and atherosclerosis.

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This study looked at specific proteins called myotubularins, which are linked to muscle and nerve disorders. Researchers found that two of these proteins, MTM-6 and MTM-9, help control a process in cells that takes in substances from outside the cell, and when they are mutated, this process gets disrupted in lab worms. Understanding how these proteins work is important, as it could lead to better insights into the diseases caused by their mutations in humans.

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Researchers studied a protein called Bam32/DAPP1 in mice to see how it affects the immune response. They found that mice without Bam32 had about a 50% decrease in B cell growth after certain immune signals. Importantly, these mice struggled to produce a specific type of antibody (IgG3), which led to a higher risk of infection from a bacterium called Streptococcus pneumoniae. This matters because understanding Bam32's role could help explain why some people have weakened immune responses, especially to certain infections.