Eric J. Lenze, Michelle Voegtle, J. Philip Miller, et al. · (2022) · "Effects of Mindfulness Training and Exercise on Cognitive Function in Older Adults" · JAMA · https://doi.org/10.1001/jama.2022.21680 · cited 143 times

Question: Summarize the published evidence on "Effects of Mindfulness Training and Exercise on Cognitive Function in Older Adults" with a citation.

Answer:
Importance: Episodic memory and executive function are essential aspects of cognitive functioning that decline with aging. This decline may be ameliorable with lifestyle interventions. Objective: To determine whether mindfulness-based stress reduction (MBSR), exercise, or a combination of both improve cognitive function in older adults. Design, Setting, and Participants: This 2 × 2 factorial randomized clinical trial was conducted at 2 US sites (Washington University in St Louis and University of California, San Diego). A total of 585 older adults (aged 65-84 y) with subjective cognitive concerns, but not dementia, were randomized (enrollment from November 19, 2015, to January 23, 2019; final follow-up on March 16, 2020). Interventions: Participants were randomized to undergo the following interventions: MBSR with a target of 60 minutes daily of meditation (n = 150); exercise with aerobic, strength, and functional components with a target of at least 300 minutes weekly (n = 138); combined MBSR and exercise (n = 144); or a health education control group (n = 153). Interventions lasted 18 months and consisted of group-based classes and home practice. Main Outcomes and Measures: The 2 primary outcomes were composites of episodic memory and executive function (standardized to a mean [SD] of 0 [1]; higher composite scores indicate better cognitive performance) from neuropsychological testing; the primary end point was 6 months and the secondary end point was 18 months. There were 5 reported secondary outcomes: hippocampal volume and dorsolateral prefrontal cortex thickness and surface area from structural magnetic resonance imaging and functional cognitive capacity and self-reported cognitive concerns. Results: Among 585 randomized participants (mean age, 71.5 years; 424 [72.5%] women), 568 (97.1%) completed 6 months in the trial and 475 (81.2%) completed 18 months. At 6 months, there was no significant effect of mindfulness training or exercise on episodic memory (MBSR vs no MBSR: 0.44 vs 0.48; mean difference, -0.04 points [95% CI, -0.15 to 0.07]; P = .50; exercise vs no exercise: 0.49 vs 0.42; difference, 0.07 [95% CI, -0.04 to 0.17]; P = .23) or executive function (MBSR vs no MBSR: 0.39 vs 0.31; mean difference, 0.08 points [95% CI, -0.02 to 0.19]; P = .12; exercise vs no exercise: 0.39 vs 0.32; difference, 0.07 [95% CI, -0.03 to 0.18]; P = .17) and there were no intervention effects at the secondary end point of 18 months. There was no significant interaction between mindfulness training and exercise (P = .93 for memory and P = .29 for executive function) at 6 months. Of the 5 prespecified secondary outcomes, none showed a significant improvement with either intervention compared with those not receiving the intervention. Conclusions and Relevance: Among older adults with subjective cognitive concerns, mindfulness training, exercise, or both did not result in significant differences in improvement in episodic memory or executive function at 6 months. The findings do not support the use of these interventions for improving cognition in older adults with subjective cognitive concerns. Trial Registration: ClinicalTrials.gov Identifier: NCT02665481.

— Source (peer-reviewed): Eric J. Lenze, Michelle Voegtle, J. Philip Miller, et al. · (2022) · "Effects of Mindfulness Training and Exercise on Cognitive Function in Older Adults" · JAMA · https://doi.org/10.1001/jama.2022.21680 · cited 143 times

Note: This summarizes published research findings. It is not individualized medical advice. For your situation, please discuss with your healthcare provider.


Anca Daniela Pinzaru, Ancuta Lupu, Tatiana Chisnoiu, et al. · (2025) · "Comparative Study of Oxidative Stress Responses in Pediatric Type 1 Diabetes and Transient Hyperglycemia" · International Journal of Molecular Sciences · doi: 10.3390/ijms26041701 · PMCID: PMC11855318 · PMID: 40004164

Question: What did the discussion section of the paper "Comparative Study of Oxidative Stress Responses in Pediatric Type 1 Diabetes and Transient Hyperglycemia" cover?

Answer:
Our research, which indicates that the serum levels of zinc and selenium in the diabetic group were significantly lower than those in the control group, underscores the need for further research in this area. This aligns with the findings of Ahmed et al., who identified that children with T1DM exhibited lower serum levels of Se and Zn than the control group [ 13 ]. Grabia et al. compared 105 T1DM patients with 65 healthy children, obtaining similar results. During diabetes onset, the levels of selenium and zinc tend to drop drastically due to hyperglycemia effects on the OS [ 14 ]. Another possible explanation for the decrease in selenium levels can be offered by the increase in selenium consumption secondary to the increase in the action of GPx, which reduces the level of free radicals created by elevated OS, as Özenç et al. explained in his research [ 15 ].

The relationship between zinc, T1DM, and OS has gained attention due to zinc’s role in the insulin complex. This has led some experts to propose a potential correlation between diabetes and zinc deficiency [ 16 , 17 ]. However, none of the patients in our study exhibited zinc deficiency, in contrast to what is observed with other essential elements. Zinc is not stored in significant amounts in the human body, so inadequate dietary intake can contribute to complications, particularly regarding OS in T1DM [ 18 , 19 ]. Despite this, there is limited research specifically addressing children and adolescents with T1DM, and the results from these studies remain inconsistent [ 17 , 19 ]. Our findings align with previous studies that found no significant difference in serum zinc levels between children and adolescents with T1DM and their healthy peers. However, it is worth noting that other studies have reported varying levels of serum zinc in children with T1DM, with some showing lower levels [ 17 , 19 ] and others showing higher levels [ 20 ]. These results suggest that while zinc may not exhibit a clear deficiency in children with T1DM, fluctuations in its levels still warrant further investigation in the context of oxidative stress.

Zinc and selenium both play crucial roles in managing oxidative stress, particularly in the context of T1DM. Zinc is an essential component of the insulin complex, and its potential deficiency has been linked to diabetic complications due to its involvement in OS processes [ 16 , 17 ]. However, none of the participants in our study exhibited zinc deficiency, aligning with findings from previous research that reported no significant differences in serum zinc levels between children and adolescents with T1DM and healthy controls. This suggests that while zinc may not show a clear deficiency in this population, its fluctuating levels still warrant further study. Indeed, studies have reported inconsistent serum zinc levels in T1DM, with some indicating lower levels [ 17 , 19 ], and others higher levels [ 20 ].

Similarly, selenium, an integral component of the enzyme GPx, plays a significant role in reducing OS by converting hydrogen and organic peroxides into less harmful substances such as alcohol and water [ 21 ]. Seleno-methionine, the primary reservoir of selenium, is not produced endogenously, which means it must be obtained through dietary sources or supplementation. Selenium’s function in reducing lipid peroxidation and mitigating ROS further underscores its importance in managing OS in T1DM [ 21 ]. Our study corroborates these findings, as we observed no significant deviations in selenium levels among participants with T1DM, suggesting that while supplementation or dietary intake may be necessary for optimal selenium status, the relationship between selenium and OS in T1DM remains complex and requires additional investigation. Selenium in pediatric research remains incompletely studied. Nie et al. analyzed over 4000 adults with diabetes. In comparison to healthy individuals, diabetic patients had notably reduced levels of serum selenium, indicating that individuals with diabetes may possess heightened metabolic requirements for selenium [ 22 ]. In the present investigation, it was observed that there were discernible disparities in selenium concentrations between preschoolers diagnosed with T1DM and their unaffected counterparts, similar to data obtained by Salmonowicz et al. after analyzing 87 children with diabetes and 41 healthy peers [ 14 , 23 ]. Selenium exhibits a notable capacity as an antioxidant, influencing the overall antioxidant equilibrium inside the human body [ 23 ]. GPx represents a highly significant selenoenzyme. The principal objective of this function is to facilitate the catalytic conversion of hydrogen peroxide into water [ 14 , 24 ]. Darenskaya observed a reduction in GPx activity in individuals with diabetes, a finding that aligns with the results of our current investigation. Furthermore, the observed percentage was approximately 20% lower in individuals with a prolonged duration of T1DM than in the early onset group. The observed outcome could lead to a diminished amount of glutathione or the deactivation of the enzyme due to heightened OS [ 25 ].

The present study investigated the activity of GPx in red blood cells, revealing a statistically significant decrease in diabetic patient compared to control participants. Dominguez et al. conducted a study that yielded the same findings, demonstrating that individuals diagnosed with T1DM exhibited lower GPx activity than their healthy counterparts. The level of GPx in children with diabetes tends to decrease compared to their siblings and parents [ 26 ]. Darmauan et al. wanted to evaluate the structure of GPx in the diabetic child, establishing step by step the moment of the installation of the deficiency. The current study indicates that blood glutathione levels are notably reduced in adolescents diagnosed with uncomplicated T1DM compared to a group of healthy volunteers matched in age and sex. Furthermore, this reduction in glutathione levels is due to a decline in the synthesizing rate. It occurs regardless of whether the rate of glutathione fractional synthesis remains unchanged or increases, depending on the level of blood glucose control [ 27 ].

Previous research has consistently shown that individuals with diabetes exhibit elevated levels of MDA in their serum compared to individuals without diabetes, a finding that is consistent with our study [ 28 , 29 ]. In line with earlier studies, our investigation also demonstrated that the lipid profile of individuals with T1DM was notably lower than that of the healthy control group. Furthermore, the levels of MDA, a key biomarker for assessing lipid peroxidation and OS, were significantly elevated in the T1DM group compared to control group. These findings align with research suggesting that elevated blood glucose levels in diabetes contribute to increased lipid peroxidation and reduced AOD, thereby exacerbating OS [ 29 ]. The significantly elevated levels of MDA observed in children with T1DM compared to those with transient hyperglycemia and the control group confirm previous studies linking oxidative damage to chronic hyperglycemia and impaired AOD mechanisms [ 28 ]. These findings reinforce the hypothesis that persistent hyperglycemia exacerbates lipid peroxidation, contributing to long-term diabetes complications.

Hyperglycemia, whether transient or persistent as in T1DM, is associated with increased oxidative stress, which is a key contributor to cellular damage [ 30 ]. The pathogenesis of OS in T1DM is described in this guideline, along with methods for management [ 31 ]. Children possess more efficient AOD mechanisms, including higher levels of endogenous antioxidants such as SOD, catalase (CAT), and GPx [ 23 ]. These enzymes help mitigate oxidative stress, potentially preventing significant alterations in oxidative markers during brief hyperglycemic episodes.

In T1DM, chronic hyperglycemia leads to sustained oxidative stress, while in transient hyperglycemia, the OS may be temporary but significant, facts that were demonstrated in a comprehensive review of OS mechanisms in pediatric conditions [ 32 ]. Bunnag et al. provided a comparative analysis of oxidative markers in transient hyperglycemia and T1DM [ 33 ]. Ceriello et al. explored the role of glycemic variability in driving OS in diabetes [ 34 ]. ROS-mediated endothelial damage promotes the activation of inflammatory pathways, increases vascular permeability, and disrupts nitric oxide (NO) bioavailability, leading to impaired vasodilation [ 35 ]. This mechanism is central to the pathogenesis of diabetic nephropathy, retinopathy, and neuropathy. Additionally, OS triggers the activation of pro-apoptotic signaling pathways, including the JNK and NF-κB pathways, which further exacerbate tissue damage and inflammation in diabetes [ 36 ]. OS plays a critical role in endothelial dysfunction, which is a key contributor to diabetic microvascular and macrovascular complications [ 37 ]. Chronic hyperglycemia leads to the excessive production of ROS through pathways such as glucose auto-oxidation, the activation of the polyol pathway, the increased formation of advanced glycation end-products (AGEs), and mitochondrial dysfunction [ 38 ]. These ROS induce oxidative damage in lipids, proteins, and DNA, impairing cellular homeostasis and leading to β-cell dysfunction [ 39 ].

However, transient hyperglycemia may not sustain these pathways long enough to induce measurable oxidative damage [ 36 , 40 ]. Furthermore, studies indicate that age-related differences in glucose metabolism could contribute to this phenomenon. Younger children have higher insulin sensitivity and a greater ability to utilize glucose efficiently, reducing OS accumulation compared to adolescents and adults [ 39 ].

The findings of this study provide insights into how OS mechanisms differ between these two conditions in pediatric patients, emphasizing the importance of early detection and management strategies. While hyperglycemia is a key driver of oxidative stress, the study suggests other contributing factors unique to T1DM, such as chronic inflammation and autoimmune processes [ 41 ]. Pro-inflammatory cytokines, common in T1DM, may exacerbate OS independently of glucose levels [ 42 ]. In transient hyperglycemia, the absence of such chronic inflammatory stimuli likely accounts for the transient nature of OS [ 41 , 42 ]. OS is exacerbated by the interaction of autoimmune and inflammatory pathways in T1DM, which leads to beta-cell death and the progression of the illness [ 43 ].

Recent studies have explored therapeutic strategies targeting OS in T1DM [ 44 , 45 ]. Natural antioxidants, such as polyphenols and vitamins, and pharmacological agents like metformin have shown potential in mitigating OS and protecting beta cells [ 46 ]. Additionally, emerging gene-editing technologies like CRISPR/Cas9 are being investigated for restoring beta-cell function by targeting redox-related pathways [ 40 ]. Another review highlights the mechanisms by which autoimmune responses intensify oxidative damage and beta-cell dysfunction, underscoring their therapeutic potential in targeting these pathways [ 47 ].

Oxidative stress-mediated mitochondrial dysfunction is a shared hallmark of asthma and T1DM. In asthma, mitochondrial damage impairs airway cell repair, while in T1DM, it compromises insulin secretion and beta-cell survival [ 48 ].

One important physiopathogenic mechanism in childhood obesity has been identified as the imbalance between antioxidants and OS [ 49 ]. Cellular damage results from this imbalance, which happens when the body’s AODs are outpaced by the generation of ROS [ 50 ]. Through hyperglycemia, hyperlipidemia, excessive caloric intake, and chronic inflammation, childhood obesity exacerbates oxidative stress. The development of metabolic syndrome and related comorbidities including insulin resistance and cardiovascular illnesses is influenced by these variables, which lead to elevated lipid peroxidation, protein carbonylation, and mitochondrial dysfunction [ 51 , 52 ]. Recent advancements focus on using novel pharmacological agents, such as GLP-1 receptor agonists, which not only promote weight loss but also appear to reduce OS by improving metabolic profiles [ 52 ]. Moreover, lifestyle interventions like diet modifications rich in antioxidants (fruits, vegetables, omega-3 fatty acids) and increased physical activity remain critical in managing OS in this population [ 53 ].

With variations in its manifestation and effects on the course of the disease, OS is a key component of the pathophysiology of both pediatric T1DM and cystic fibrosis (CF). Given that OS is linked to inflammatory pathways, organ damage, and metabolic problems, this is especially important when comparing these two disorders and their associations with temporary hyperglycemia [ 54 ]. To prevent metabolic complications, continuous glucose monitoring (CGM) has proven to be an effective tool, especially in pediatric patients with T1DM, offering a more accurate and immediate picture of glycemic trends compared to traditional finger-stick tests [ 55 ].

In the pathophysiology of T1DM and chronic hepatitis, OS plays a crucial role. Both conditions are characterized by persistent inflammation and immunological activity, which contribute to the overproduction of ROS [ 55 ]. These ROS cause damage to cellular structures, including lipids, proteins, and DNA, leading to cellular dysfunction and accelerated disease progression. In T1DM, chronic hyperglycemia exacerbates oxidative stress, creating a feedback loop that further enhances inflammation and immune activation. Similarly, in chronic hepatitis, prolonged viral infection or autoimmune responses trigger continuous inflammatory processes, which also promote ROS generation [ 56 ]. This sustained oxidative damage can impair organ function and contribute to the development of complications such as vascular damage, insulin resistance, and liver fibrosis. The accumulation of ROS in both conditions highlights the importance of AOD mechanisms, which can mitigate some of the oxidative damage and potentially slow disease progression [ 56 ].

Many variables that affect the severity and consequences of the illness, particularly in those with pre-existing disorders like diabetes, have come to light as a result of COVID-19 [ 57 ]. OS is a key factor in the pathophysiology of both diabetes and COVID-19, according to research. When the two diseases coexist, the body frequently faces additional difficulties that worsen tissue damage, inflammation, and immunological dysfunction [ 58 ].

The study provides a comparative analysis of OS markers in T1DM and transient hyperglycemia, highlighting key differences in their pathophysiology. The pediatric focus offers valuable insights into early-stage disease processes.

— Source (discussion, peer-reviewed): Anca Daniela Pinzaru, Ancuta Lupu, Tatiana Chisnoiu, et al. · (2025) · "Comparative Study of Oxidative Stress Responses in Pediatric Type 1 Diabetes and Transient Hyperglycemia" · International Journal of Molecular Sciences · doi: 10.3390/ijms26041701 · PMCID: PMC11855318 · PMID: 40004164
License: CC-BY. Retrieved from PubMed Central full text.

Note: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team.


Denis E. O’Donnell, Casey E. Ciavaglia, J. Alberto Neder · (2014) · "When Obesity and Chronic Obstructive Pulmonary Disease Collide. Physiological and Clinical Consequences" · Annals of the American Thoracic Society · https://doi.org/10.1513/annalsats.201312-438fr · cited 102 times

Question: What does the peer-reviewed literature show about "When Obesity and Chronic Obstructive Pulmonary Disease Collide. Physiological and Clinical Consequences"? Cite a published source.

Answer:
In many parts of the world, the prevalence of both chronic obstructive pulmonary disease (COPD) and obesity is increasing at an alarming rate. Such patients tend to have greater respiratory symptoms, more severe restriction of daily activities, poorer health-related quality of life, and greater health care use than their nonobese counterparts. Physiologically, increasing weight gain is associated with lung volume reduction effects in both health and disease, and this should be considered when interpreting common pulmonary function tests where lung volume is the denominator, such as FEV1/FVC and the ratio of diffusing capacity of carbon monoxide to alveolar volume, or indeed when evaluating the physiological consequences of emphysema in obese individuals. Contrary to expectation, the presence of mild to moderate obesity in COPD appears to have little deleterious effect on respiratory mechanics and muscle function, exertional dyspnea, and peak symptom-limited oxygen uptake during cardiopulmonary exercise testing. Thus, in evaluating obese patients with COPD reporting activity restriction, additional nonpulmonary factors, such as increased metabolic loading, cardiocirculatory impairment, and musculoskeletal abnormalities, should be considered. Care should be taken to recognize the presence of obstructive sleep apnea in obese patients with COPD, as effective treatment of the former condition likely conveys an important survival advantage. Finally, morbid obesity in COPD presents significant challenges to effective management, given the combined effects of erosion of the ventilatory reserve and serious metabolic and cardiovascular comorbidities that collectively predispose to an increased risk of death from respiratory failure.

— Source (peer-reviewed): Denis E. O’Donnell, Casey E. Ciavaglia, J. Alberto Neder · (2014) · "When Obesity and Chronic Obstructive Pulmonary Disease Collide. Physiological and Clinical Consequences" · Annals of the American Thoracic Society · https://doi.org/10.1513/annalsats.201312-438fr · cited 102 times

Note: This summarizes published research findings. It is not individualized medical advice. For your situation, please discuss with your healthcare provider.


Arthur Tarricone, Allen Gee, Lee C. Rogers, et al. · (2026) · "Tibial Osteodistraction Angiogenesis for Diabetic Foot Ischemia: A Systematic Review and Meta‐Analysis" · Wound Repair and Regeneration · doi: 10.1111/wrr.70130 · PMCID: PMC12895301 · PMID: 41674377

Question: What did the discussion section of the paper "Tibial Osteodistraction Angiogenesis for Diabetic Foot Ischemia: A Systematic Review and Meta‐Analysis" cover?

Answer:
The results of this study suggest that ODA is a promising treatment option for patients that have wounds with impaired perfusion and are at a high risk of amputation. Across the literature, we found ODA improved healing rates and reduced the risk of major amputation and death. The pooled data show that 91% of patients treated with ODA experienced successful wound healing in 7–53 days. Only 2% of the patients required amputation, and only 4% died. In addition, the findings of this study showed that cytokines were significantly increased following the ODA procedure.

Amputation is one of the most feared complications of diabetes [ 30 ]. Below or above‐the‐knee amputation dramatically reduces quality of life [ 31 , 32 ], reduces the ability to live independently [ 33 , 34 ], and reduces life expectancy [ 35 , 36 ]. Lower extremity amputations also have profoundly negative psychological and social implications [ 37 ] that lead to depression, anxiety, loss of self‐esteem, and isolation [ 38 ]. The emotional and financial burden of an amputee often falls on family members.

Gavriil Ilizarov's pioneering work, arising from an accidental discovery, defined distraction osteogenesis. This technique harnesses the intrinsic regenerative capacity of bone by creating an osteotomy and gradually separating the segments. This controlled separation stimulates the production of new bone tissue, concurrent with increased vascularization in the surrounding soft tissues [ 39 , 40 ]. Osteodistraction Angiogenesis is based on a similar principle to enhance perfusion in individuals with ischemia. This mechanical distraction initiates a cascade of biochemical signals that promote tissue regeneration, including angiogenesis, modulation of the inflammatory response, and immunomodulatory effects [ 12 , 41 , 42 ]. The studies included in this review demonstrated an increase in perfusion to the foot based on serial arterial Dopplers, transcutaneous oxygen measurements (TCOM), and computer tomography angiography (CTA). Evaluations of pre vs. post‐distraction consistently demonstrate improved perfusion to the foot [ 12 , 16 , 25 , 28 , 29 , 43 ].

The challenges in treating PAD and preventing amputations in individuals with diabetes are further compounded by the complex vascular anatomy of the lower leg and foot. Individuals with diabetes‐related PAD usually have multiple stenoses or occlusions of the three principal arteries below the knee, which makes surgical revascularization technically challenging [ 44 , 45 ]. Even when successful, re‐occlusion after revascularization is very common [ 46 ]. In patients with diabetic foot ischemia, re‐occlusion or re‐stenosis of the treated arteries occurs frequently, limiting long‐term success. The success of revascularization for wound healing is dependent upon restoring adequate perfusion to the affected angiosomes, particularly where there is a wound [ 44 , 47 ]. If perfusion cannot be optimised, healing is impaired, and the risk of amputation increases. Studies have shown a clear correlation between the number of patent arteries (out of three) supplying the foot and the likelihood of amputation. When two or three arteries are open, the amputation rate is significantly lower compared with situations where only one or no arteries are patent. In many cases, only one or two of the arteries can be successfully treated. Truong and colleagues reported that if two or three vessels are patent to the foot, only 23% of patients will require leg amputation [ 47 ]. If there are no vessels or only one vessel that supplies the foot, 61% will require leg amputation. Patients with 0–1 arteries that extend into the foot were 2.5 times (1.4–19.5, p = 0.01) more likely to require amputation of the leg. In addition, if there is successful revascularization to an artery but it does not supply blood to the wound's angiosome, the risk of death, poor healing, amputation is 1.8 to 2.6 times higher [ 44 ].

In contrast to traditional revascularization techniques that focus on opening specific arteries, the ODA technique offers a unique advantage. ODA stimulates angiogenesis throughout the foot, including areas not directly supplied by the major arteries. This diffuse angiogenic effect may improve perfusion to all areas of the foot, even in the presence of multi‐vessel disease. Furthermore, ODA has been shown to promote angiogenesis in the contralateral limb (untreated side), potentially offering benefits for patients with bilateral PAD. This broader angiogenic effect may explain why ODA has shown promising results in preventing amputations and improving outcomes in patients with limb‐threatening ischemia (sometimes referred to as critical limb ischemia).

There are important limitations involving the existing studies and our analysis. First, there was significant heterogeneity among the studies that were included in terms of study design, patient populations, interventions, and outcome measures. Most of the studies were retrospective, and there were only two prospective cohort studies. There were no randomised clinical trials. Most studies only provided 1 year of follow‐up. None of the studies provided any angiographic classification of PAD before or after surgery. Therefore, it was difficult to understand the severity of PAD within and between studies. These studies commonly represented a cross section of diabetic foot wound complexity based on the Wagner or UT ulcer classification [ 48 ]. None of the studies report the frequency or level of foot amputations. All studies reviewed were conducted in China, where there may be differences in the standard of care for wound management and vascular surgery compared with the US and Europe.

While there are promising endpoints that can be extracted from this analysis, study heterogeneity limits the ability to pool data and draw definitive conclusions. The overall quality of the studies that were included in this meta‐analysis was variable, with some studies lacking detailed reporting of methodology and exhibiting potential risks of bias. Most studies were conducted in single centers with limited sample sizes, and all studies were conducted in China without incorporation of any western cohorts; therefore, both factors play the potential in limiting the generalizability of the findings to other populations. Publication bias may also be present, as studies with positive results are more likely to be published. This could lead to an overestimation of the true effect of ODA. This review also was limited in the types of studies, with many retrospective studies, two prospective trials, and no randomised controlled trials. With these considerations in mind, it is important to view the results of this study as hypothesis generating as opposed to concrete evidence for ODA use. Lastly, the number of included studies was relatively small, and the follow‐up periods were generally short. Larger, long‐term studies are needed to confirm these findings and assess the durability of ODA's effects.

— Source (discussion, peer-reviewed): Arthur Tarricone, Allen Gee, Lee C. Rogers, et al. · (2026) · "Tibial Osteodistraction Angiogenesis for Diabetic Foot Ischemia: A Systematic Review and Meta‐Analysis" · Wound Repair and Regeneration · doi: 10.1111/wrr.70130 · PMCID: PMC12895301 · PMID: 41674377
License: CC-BY. Retrieved from PubMed Central full text.

Note: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team.


Xiaodong Zheng, Dun X. Tan, Andrew C. Allan, et al. · (2017) · "Chloroplastic biosynthesis of melatonin and its involvement in protection of plants from salt stress" · Scientific Reports · https://doi.org/10.1038/srep41236 · cited 201 times

Question: What does the peer-reviewed literature show about "Chloroplastic biosynthesis of melatonin and its involvement in protection of plants from salt stress"? Cite a published source.

Answer:
of the purified recombinant MzASMT9 protein for melatonin synthesis were 500 μM and 12 pmol/min·mg protein, respectively. Arabidopsis ectopically-expressing MzASMT9 possessed improved melatonin level. Importantly, the MzASMT9 gene was found to be upregulated by high light intensity and salt stress. Increased melatonin due to the highly-expressed MzASMT9 resulted in Arabidopsis lines with enhanced salt tolerance than wild type plants, as indicated by reduced ROS, lowered lipid peroxidation and enhanced photosynthesis. These findings have agricultural applications for the genetic enhancement of melatonin-enriched plants for increasing crop production under a variety of unfavorable environmental conditions.

— Source (peer-reviewed): Xiaodong Zheng, Dun X. Tan, Andrew C. Allan, et al. · (2017) · "Chloroplastic biosynthesis of melatonin and its involvement in protection of plants from salt stress" · Scientific Reports · https://doi.org/10.1038/srep41236 · cited 201 times

Note: This summarizes published research findings. It is not individualized medical advice. For your situation, please discuss with your healthcare provider.


Jessica Ellis, Carolyn M. Brown, Brian Barger, et al. · (2019) · "Influence of Maternal Obesity on Labor Induction: A Systematic Review and Meta‐Analysis" · Journal of Midwifery & Women s Health · https://doi.org/10.1111/jmwh.12935 · cited 136 times

Question: What does the peer-reviewed literature show about "Influence of Maternal Obesity on Labor Induction: A Systematic Review and Meta‐Analysis"? Cite a published source.

Answer:
INTRODUCTION: Studies have shown that women with obesity have longer labors. The purpose of this systematic review and meta-analysis is to examine existing evidence regarding labor induction in women with obesity, including processes and outcomes. The primary outcome was cesarean birth following labor induction. Secondary outcomes were the timing and dosage of prostaglandins, the success of mechanical cervical ripening methods, and synthetic oxytocin dose and timing. METHODS: statistics. We also calculated fixed-effect models to estimate pooled relative risks and weighted mean differences. RESULTS: Ten cohort studies met inclusion criteria; 8 studies had data available for a meta-analysis of the primary outcome. Cesarean birth was more common among women with obesity compared with women of normal weight following labor induction (Mantel-Haenszel fixed-effect odds ratio, 1.82; 95% CI, 1.55-2.12; P < .001). Maternal obesity was associated with a longer time to birth, higher doses of prostaglandins, less frequent success of cervical ripening methods, and higher dose of synthetic oxytocin, as well as a longer time to birth after oxytocin use. DISCUSSION: Women with obesity are more likely than women with a normal weight to end labor induction with cesarean birth. Additionally, women with obesity require longer labor inductions involving larger, more frequent applications of both cervical ripening methods and synthetic oxytocin.

— Source (peer-reviewed): Jessica Ellis, Carolyn M. Brown, Brian Barger, et al. · (2019) · "Influence of Maternal Obesity on Labor Induction: A Systematic Review and Meta‐Analysis" · Journal of Midwifery & Women s Health · https://doi.org/10.1111/jmwh.12935 · cited 136 times

Note: This summarizes published research findings. It is not individualized medical advice. For your situation, please discuss with your healthcare provider.


Tanja Jaeggi, Guus A. M. Kortman, Diego Moretti, et al. · (2014) · "Iron fortification adversely affects the gut microbiome, increases pathogen abundance and induces intestinal inflammation in Kenyan infants" · Gut · https://doi.org/10.1136/gutjnl-2014-307720 · cited 609 times

Question: Summarize the published evidence on "Iron fortification adversely affects the gut microbiome, increases pathogen abundance and induces intestinal inflammation in Kenyan infants" with a citation.

Answer:
BACKGROUND: In-home iron fortification for infants in developing countries is recommended for control of anaemia, but low absorption typically results in >80% of the iron passing into the colon. Iron is essential for growth and virulence of many pathogenic enterobacteria. We determined the effect of high and low dose in-home iron fortification on the infant gut microbiome and intestinal inflammation. METHODS: We performed two double-blind randomised controlled trials in 6-month-old Kenyan infants (n=115) consuming home-fortified maize porridge daily for 4 months. In the first, infants received a micronutrient powder (MNP) containing 2.5 mg iron as NaFeEDTA or the MNP without iron. In the second, they received a different MNP containing 12.5 mg iron as ferrous fumarate or the MNP without the iron. The primary outcome was gut microbiome composition analysed by 16S pyrosequencing and targeted real-time PCR (qPCR). Secondary outcomes included faecal calprotectin (marker of intestinal inflammation) and incidence of diarrhoea. We analysed the trials separately and combined. RESULTS: At baseline, 63% of the total microbial 16S rRNA could be assigned to Bifidobacteriaceae but there were high prevalences of pathogens, including Salmonella Clostridium difficile, Clostridium perfringens, and pathogenic Escherichia coli. Using pyrosequencing, +FeMNPs increased enterobacteria, particularly Escherichia/Shigella (p=0.048), the enterobacteria/bifidobacteria ratio (p=0.020), and Clostridium (p=0.030). Most of these effects were confirmed using qPCR; for example, +FeMNPs increased pathogenic E. coli strains (p=0.029). +FeMNPs also increased faecal calprotectin (p=0.002). During the trial, 27.3% of infants in +12.5 mgFeMNP required treatment for diarrhoea versus 8.3% in -12.5 mgFeMNP (p=0.092). There were no study-related serious adverse events in either group. CONCLUSIONS: In this setting, provision of iron-containing MNPs to weaning infants adversely affects the gut microbiome, increasing pathogen abundance and causing intestinal inflammation. TRIAL REGISTRATION NUMBER: NCT01111864.

— Source (peer-reviewed): Tanja Jaeggi, Guus A. M. Kortman, Diego Moretti, et al. · (2014) · "Iron fortification adversely affects the gut microbiome, increases pathogen abundance and induces intestinal inflammation in Kenyan infants" · Gut · https://doi.org/10.1136/gutjnl-2014-307720 · cited 609 times

Note: This summarizes published research findings. It is not individualized medical advice. For your situation, please discuss with your healthcare provider.