Hasil untuk "Diseases of the endocrine glands. Clinical endocrinology"

Le-yi Zhang, Le-yi Zhang, Le-yi Zhang et al.

Diabetic Retinopathy (DR) is a leading cause of vision loss in diabetic patients, driven by oxidative stress, inflammation, and vascular abnormalities. Recent studies highlight amino acid metabolism abnormalities, particularly in glutamate, arginine, and tryptophan, as critical factors in DR pathogenesis. Preclinical evidence suggests that these metabolic disturbances may contribute to retinal neurodegeneration and vascular damage, offering potential new targets for therapy. Natural plant-derived compounds, such as flavonoids, catechins, and alkaloids, have been shown in animal and cell culture studies to regulate amino acid metabolism and may offer therapeutic potential for DR, although clinical validation remains limited. These compounds exhibit antioxidant, anti-inflammatory, and neuroprotective properties. Flavonoids improve amino acid accumulation, reduce oxidative stress, and protect retinal cells, while catechins enhance amino acid synthesis and redox balance. Alkaloids like berberine regulate nitric oxide synthesis, improving retinal microcirculation and endothelial function. In DR, glutamate excess activates NMDA receptors, leading to retinal neuronal toxicity, while arginine and tryptophan metabolism abnormalities further disrupt vascular and immune function. Natural drugs targeting these pathways could alleviate oxidative stress, inflammation, and retinal damage. However, challenges remain in clinical application, including low bioavailability and variability in product quality. Future research should focus on multi-omics integration, personalized medicine, and clinical trials to establish robust evidence for the use of natural drugs in DR treatment, ultimately improving long-term visual outcomes and quality of life.

Yan‐li Zhao, Yang Ou

ABSTRACT Objective To clarify the link between environmental pollution and diabetes risk by focusing on pancreatic β‐cells as key targets of environmental insults, with emphasis on the role of endocrine‐disrupting chemicals (EDCs) in pancreatic dysfunction and diabetes pathogenesis. Methods This narrative review synthesises recent research on EDCs, focusing on their effects on β‐cells. The literature search included studies in English on EDCs, diabetes, and β‐cell function, utilising Boolean operators to refine the search. Results EDCs impair β‐cell function through mechanisms such as oxidative stress, mitochondrial damage, and epigenetic changes. These pollutants disrupt insulin synthesis, secretion, and β‐cell survival, which is distinct from their general metabolic effects. Additionally, EDCs may interact synergistically with traditional diabetes risk factors, such as high‐fat diets, amplifying the risk of diabetes. Conclusion Environmental pollutants play a significant role in β‐cell dysfunction and diabetes, offering new directions for research and prevention.

Patricio H. Contreras, Henrik Falhammar, Henrik Falhammar

Evidence synthesisObesity is a state of subtle hypercortisolism accompanied by leptin and insulin resistance. Serum total cortisol concentration is normal or slightly subnormal in obese subjects. However, they have high cortisol production rates. Reduced concentrations of serum cortisol-binding globulin caused by hyperinsulinemia explain this paradox. Elevated free cortisol concentrations act on the adipose cells of these patients due to excess adrenal cortisol secretion, as well as to high adipocyte expression of 11-beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1). CRF1 and ACTH blockers (such as crinecerfont and atumelnant, respectively) may replace leptin action on the adrenal axis by reducing adrenal cortisol excess in individuals with obesity.ContextIndividuals with obesity experience a subtle hypercortisolism secondary to leptin resistance. Weight loss is commonly followed by a weight rebound, likely provoked by residual leptin resistance. Since leptin inhibits the adrenal axis, leptin resistance induces a hypersecretion of cortisol, promoting chronic, pathological lipolysis of white adipose tissue. The latter situation leads to lean organ steatosis, muscle and liver insulin resistance, and β-cell apoptosis. So, there is an urgent need to restore adrenal inhibition in obese individuals.Evidence acquisitionWe searched PubMed articles and included them if relevant.ConclusionsIndividuals with obesity and high levels of adipose insulin resistance may benefit from CRF1/ACTH inhibitors, reducing ACTH secretion or its action. A reduction in their adipose resistance index may lead to diminished lean organ steatosis and reduced appetite due to a decrease in orexigenic signals, mainly free cortisol and insulin.

Matthieu Clauss, Claire Puissant, Nasser Ezzatkhah Bastani et al.

BackgroundHormonal and metabolic responses to high protein intake are not well understood. The aims of this study were to compare the metabolic and hormonal responses to isocaloric intakes of whey protein alone versus carbohydrate alone. Additionally, we measured urinary nitrogen excretion as a marker of protein degradation.MethodsFourteen young, healthy, moderate-to-well-trained participants (VO2max 50.6 ± 2.9 mL·kg-1·min-1; mean ± SEM) reported in the morning after an overnight fast. In a double-blinded, randomized, balanced cross-over design, participants consumed isoenergetic test drinks containing either 1.2 g·kg-1 of whey protein alone (PRO) or carbohydrate alone (CHO) on separate days. They recorded their dietary intake the day before and during the intervention to repeat them across the second trial day. Blood samples were collected at regular intervals after drink ingestion. Urine was collected throughout the testing period in six consecutive batches.ResultsAfter CHO intake, plasma glucose levels increased, and certain plasma amino acid concentrations decreased. Following PRO intake, plasma glucose decreased, and plasma amino acids increased. Insulin concentrations increased following ingestion of both CHO and PRO (time effect, p<0.001), with a greater increase in CHO (drink effect, p<0.001). Plasma GLP-1 and GIP concentrations increased in both conditions (time effect, p<0.001). Plasma GLP-1 increased more in PRO than in CHO (drink effect, p<0.001), whereas plasma GIP increased more in CHO than in PRO (drink effect, p<0.001). Urinary nitrogen excretion over the 24 hours following drink ingestion was significantly higher in PRO (p<0.001), particularly between 2 to 8 hours after intake (p<0.001).ConclusionsCHO increased plasma insulin more than PRO. The PRO induced insulin response was independent of glucose and mediated by the increase in plasma amino acids and GLP-1. Interestingly, the GLP-1 response was larger following PRO and remained elevated after 240 minutes, whereas the GIP response was larger following CHO. Additionally, protein-only ingestion increased urinary nitrogen excretion, mainly between 2 to 8 hours after intake, with elevated excretion persisting up to 24 hours.

Melanie Rodacki, Karina Ribeiro Silva, Debora Batista Araujo et al.

ABSTRACT Type 1 diabetes (TID) is a chronic disease caused by autoimmune destruction of pancreatic β-cells, that progresses in three stages: 1) stage 1: β-cell autoimmunity + normoglycemia; 2) stage 2: β-cell autoimmunity + mild dysglycemia; 3) stage 3: symptomatic disease + hyperglycemia. Interventions to prevent or cure T1D in the various stages of the disease have been pursued and may target the prevention of the destruction of β cells, regression of insulitis, preservation or recovery of β cells residual mass. Some therapies show promising results that might change the natural history and the approach to patients with T1D in the next few years. Teplizumab, a humanized monoclonal antibody that binds to CD3, was recently approved in the USA to delay Stage 3 T1D in individuals ≥ 8 years of age. Other non-cellular immunomodulatory therapies, both antigen-specific and non-specific, have shown interesting results either in patients with stage 2 or recent onset stage 3 T1D. Cell therapies such as non-myeloablative transplantation of autologous hematopoietic stem cells, mesenchymal stem cells, and tolerogenic dendritic cells have been also studied in these individuals, aiming immunomodulation. Stem cell-derived islet replacement therapy is promising for patients with long-standing T1D, especially with asymptomatic hypoglycemia not resolved by technology. This review aimed to provide updated information on the main immunomodulatory agents and cell therapy options for type 1 diabetes.

Ali Akbar Soleimani, Nafiseh Shokri, Mohammad Elahimanesh et al.

Abstract Background Metformin (Met) and dexamethasone (Dexa) are known to reduce blood sugar levels and anti‐inflammatory effects, respectively. Based on the acceleration of atherosclerosis process in diabetes, the β‐arrestin 2 (BARR2) gene and protein expression levels were evaluated in vascular smooth muscle cells (VSMCs) treated with Met and Dexa in high glucose conditions in this study. Methods and Materials Human VSMCs were cultured in Dulbecco's Modified Eagle Medium/Nutrient Mixture F‐12 (DMEM‐F12) medium and, were treated with different values of Met (1 mM, 5 mM and 7 mM) and Dexa (10−7 M, 10−6 M and 10−5 M) in 24‐ and 48‐h periods. The BARR2 gene and protein expression levels were identified with RT‐qPCR and western blotting techniques, respectively. The signalling axes were predicted from gene network made using Cytoscape software and, were annotated with Gene Ontology. Results The BARR2 gene and protein expression levels reduced in VSMCs treated with Dexa and Met after 24‐ and 48‐h periods. These results were more changed after 48 h. Furthermore, many BARR2‐related signalling axes were found from the network genes. Conclusion Met and Dexa suppressed the BARR2 protein and gene expression levels in the VSMCs. Moreover, the gene network suggested some the cellular signalling axes related to BARR2 that may be affected by Met and Dexa.

Chizuru Ito, Tohru Mutoh, Kiyotaka Toshimori

Abstract Purpose The purpose of this study is to confirm whether in vitro fertilization (IVF) with spermatozoa from Odf4‐deficient infertile males (Odf4−/− spermatozoa) can lead to the development of zygotes, which was reported in a previous in vivo study. Methods In vitro capacitation and IVF were performed using Odf4−/− spermatozoa in a small drop of TYH medium with pyruvate and glucose, for 60 min or up to 4 days. A capacitation test was performed by immunoblotting using an anti‐p‐Tyr antibody. A sperm movement test was performed using a computer‐assisted sperm motility analysis system (SMAS). An IVF fertilization test was also performed to evaluate zygote production. Videos were taken by a DMi8 stereomicroscope equipped with a high‐speed camera. Results In in vitro condition, Odf4−/− spermatozoa with hairpin flagella harboring large cytoplasmic droplets (CDs) underwent capacitation, about 30% of large CDs were removed from spermatozoa, and the flagella became straight (capacitation test). The Odf4−/− spermatozoa with straight flagella swam forward (movement test) and fertilized Odf4+/+ oocytes, which eventually developed into zygotes (fertilization test). Conclusions By conventional IVF, spermatozoa from Odf4‐deficient male mice can fertilize oocytes that then develop into zygotes. These findings can be translated to human males with infertility caused by ODF4 deficiency.

V. Hoperia, O. Mostiuk, A. Dinets et al.

Background. The Warthin-like variant of papillary thyroid carcinoma (WLPTC) is a rare papillary thyroid carcinoma that is considered to be a subtype of the oncocytic variant. Purpose of the study: to present the diagnostic and clinical features, the oncological and surgical management of a patient with WLPTC as well as its discussion with other relevant studies. Materials and methods. We report a case of Warthin-like papillary thyroid carcinoma in a 31-year-old woman with Hashimoto thyroiditis. Results. The patient was admitted to the hospital with the presence of a node in the thyroid gland. Thyroid ultrasound showed a 24-mm nodule with oval shape and irregular contours in the left lobe. A fine-needle aspiration biopsy was performed, and a diagnosis of papillary thyroid carcinoma was made. The patient underwent thyroidectomy, bilateral modified and central neck dissection, lymphadenectomy. Histopathological examination suggested a WLPTC coexisting with chronic thyroiditis, metastases to the lymph nodes 2, 3, 4 on the left and 6 neck compartments. The patient underwent postoperative I131 ablation therapy. Conclusions. WLPTC is a recently described variant of papillary thyroid cancer that is frequently associated with lymphocytic thyroiditis. The correct cytological and histomorphological features are of utmost importance to render the diagnosis of WLPTC for better management. A surgical and postoperative treatment is identical to that in classic differentiated thyroid cancer, having a favorable outcome due to a low recurrence rate. A surgical management should be thyroidectomy and dissection of central neck compartment as well as lateral dissection in cases of suspicions for metastases in the lymph nodes or metastases confirmed preoperatively by a fine-needle aspiration biopsy.

Zhong-Zhong Chen, Yun-Qian Gao, Hua Xie et al.

Abstract. Objective:. To investigate the roles of transcription factors (TFs) in the etiology of complex human birth defects, including neural tube defects (NTDs), congenital heart diseases (CHDs), and hypospadias. Methods:. We examined the overlap of genetically associated genes among NTDs, CHDs, and hypospadias. We then compared the expression profiles of these diseases based on all the detected genes and disease-associated TFs. The differentially expressed TFs that we obtained were further subjected to functional enrichment analysis to elucidate their role in the development of these birth defects. Results:. TF genes were significantly enriched in complex birth defects (P = 5.95 × 10−24). NTDs, CHDs, and hypospadias showed distinct gene expression profiles compared with the controls. Although TFs could not efficiently separate CHDs from normal subjects, distinct gene expression profiles of TFs could distinguish NTDs and hypospadias from controls. Differentially expressed TFs can be used to characterize NTDs, hypospadias, and controls. The enriched TFs in biological processes (BPs) reflected the different morphological processes of NTDs, CHDs, and hypospadias. Conclusions:. This study indicates that abnormal expression patterns of specific TFs may disrupt the normal requirements for developmental equilibrium through the related BPs. The investigation of genetically associated genes and gene expression profiles for the three different complex birth defects provides new insights into how the dysregulation of TFs influences their developmental process.

Yang Liu, Guohua Li, Nafei Guo et al.

ObjectiveWe aimed to determine the association between maternal characteristics and isolated maternal hypothyroxinemia (IMH).MethodsPregnancies registered at Shanghai First Maternity and Infant Hospital between January 2014 and September 2020 were included in this cross-sectional study. IMH was defined as free thyroxine (FT4) levels below the 10th percentile with TSH within the normal reference range. Multivariate logistic regression models were used to identify potential risk factors for IMH, including demographic information, anthropometric measurements and nutritional status.ResultsA total of 54586 singleton pregnancies were included, involving 6084 women with IMH and 48502 euthyroid women. Multivariate logistic regression analyses showed that the variables for women with ages ≥35 (adjusted OR = 1.30, 95% CI:1.20–1.40), non-local residence (adjusted OR = 1.16, 95% CI:1.09–1.23), multiparas (adjusted OR = 1.11, 95% CI:1.03–1.21), pre-pregnancy overweight (adjusted OR = 1.37, 95% CI:1.27–1.49) or obesity (adjusted OR = 1.35, 95% CI:1.18–1.54), and iron deficiency (adjusted OR = 1.27, 95% CI:1.20–1.35) were independent risk factors for IMH in the overall study population, which were identical to those in the first trimester subgroup.ConclusionsMaternal characteristics were associated with the onset of IMH. Maternal age, residence of origin, parity, pre-pregnancy body mass index (BMI) and iron status should be comprehensively considered to evaluate the risk of IMH, according to which obstetricians could determine an optimal assessment time for thyroid function.

Takuro Okamura, Hiroshi Okada, Hiroshi Okada et al.

Background and AimsTo understand the role of microRNAs in muscle atrophy caused by androgen-depletion, we performed microarray analysis of microRNA expression in the skeletal muscles of Sham, orchiectomized (ORX), and androgen-treated ORX mice.MethodsTo clarify role and mechanisms of let-7e-5p in the muscle, the effect of let-7e-5p overexpression or knockdown on the expression of myosin heavy chain, glucose uptake, and mitochondrial function was investigated in C2C12 myotube cells. Moreover, we examined serum let-7e-5p levels among male subjects with type 2 diabetes.ResultsWe found that the expression of the miRNA, lethal (let)-7e-5p was significantly lower in ORX mice than that in Sham mice (p = 0.027); however, let-7e-5p expression in androgen-treated ORX mice was higher (p = 0.047). Suppression of let-7e-5p significantly upregulated the expression of myosin heavy chain, glucose uptake, and mitochondrial function. Real-time PCR revealed a possible regulation involving let-7e-5p and Igf2bp2 mRNA and protein in C2C12 cells. The serum let-7e-5p levels were significantly lower, which might be in compensation, in subjects with decreased muscle mass compared to subjects without decreased muscle mass. Let-7e-5p downregulates the expression of Igf2bp2 in myotube cells and inhibits the growth of the myosin heavy chain.ConclusionsBased on our study, serum level of let-7e-5p may be used as a potential diagnostic marker for muscle atrophy.

Livia Odagiu, Livia Odagiu, Julia May et al.

The nuclear orphan receptors NR4A1, NR4A2, and NR4A3 are immediate early genes that are induced by various signals. They act as transcription factors and their activity is not regulated by ligand binding and are thus regulated via their expression levels. Their expression is transiently induced in T cells by triggering of the T cell receptor following antigen recognition during both thymic differentiation and peripheral T cell responses. In this review, we will discuss how NR4A family members impact different aspects of the life of a T cell from thymic differentiation to peripheral response against infections and cancer.

Yukihiro Fujita, Yukihiro Fujita, Kuralay K. Atageldiyeva et al.

ObjectiveA low-carbohydrate diet (LC) can be beneficial to obese subjects with type2 diabetes mellitus (T2DM). Sodium-glucose cotransporter 2 inhibitor (SGLT2i) presents prompt glucose-lowering effects in subjects with T2DM. We investigated how LC and SGLT2i could similarly or differently influence on the metabolic changes, including glucose, lipid, and ketone metabolism in lean insulinopenic Akita mice. We also examined the impacts of the combination.MethodsMale Akita mice were fed ad libitum normal-carbohydrate diet (NC) as a control or low-carbohydrate diet (LC) as an intervention for 8 weeks with or without SGLT2i treatment. Body weight and casual bold glucose levels were monitored during the study, in addition to measuring TG, NEFA, and ketone levels. We quantified gene expressions involved in gluconeogenesis, lipid metabolism and ketogenesis in the liver and the kidney. We also investigated the immunostaining analysis of pancreatic islets to assess the effect of islet protection.ResultsBoth LC and SGLT2i treatment reduced chronic hyperglycemia. Moreover, the combination therapy additionally ameliorated glycemic levels and preserved the islet morphology in part. LC but not SGLT2i increased body weight accompanied by epididymal fat accumulation. In contrast, SGLT2i, not LC potentiated four-fold ketone production with higher ketogenic gene expression, in comparison with the non-treated Akita mice. Besides, the combination did not enhance further ketone production compared to the SGLT2i alone.ConclusionsOur results indicated that both LC and SGLT2i reduced chronic hyperglycemia, and the combination presented synergistic favorable effects concomitantly with amelioration of islet morphology, while the combination did not enhance further ketosis in Akita mice.

Huimin Ji, Huimin Ji, Huimin Ji et al.

Although the rapid development of high-throughput sequencing has led to the identification of a large number of truncated or mutated steroid hormone receptor (SHR) variants, their clinical relevance remains to be defined. A platform for functional analysis of these SHR variants in cells would be instrumental for better assessing their impact on normal physiology and SHR-associated diseases. Here we have developed a new reporter system that allows rapid and accurate assessment of the transcriptional activity of SHR variants in cells. The reporter is a single construct containing a firefly luciferase reporter gene, whose expression is under the control of a promoter with multiple steroid hormone responsive elements, and a Renilla luciferase reporter gene, that is constitutively expressed under the control of an internal ribosome entry site (IRES) and is not regulated by steroid hormones. The corresponding SHR (wildtype or mutant/variant) is also expressed from the same construct. Using this improved reporter system, we revealed a large spectrum of transactivation activities within a set of previously identified mutations and variations of the androgen receptor (AR), the estrogen receptor α (ERα) and the glucocorticoid receptor (GR). This novel reporter system enables functional analysis of SHR mutants and variants in physiological and pathological settings, offering valuable preclinical, or diagnostic information for the understanding and treatment of associated diseases.

Venkatesan Radha, Bhuvanagiri Ramya, Sundaramoorthy Gopi et al.

Neonatal diabetes mellitus (NDM) is a monogenic form of diabetes mellitus that occurs in the first 6 months of life. It is a rare condition with a prevalence of 1 in 100,000–500,000 live births. We report a 3-month-old girl child with high blood glucose levels. She was diagnosed with diabetes mellitus during the 28th day of life and was on treatment with insulin. She was admitted for the control of high blood glucose levels during which she was started on multiple daily insulin treatment, but the control had been poor. As the age of onset is <6 months of life, genetic analysis has been done. It revealed the presence of a heterozygous mutation p. Gly334Val (p. G334V) in KCNJ11 gene which confirmed the diagnosis of NDM. The child was successfully shifted from insulin to sulfonylureas, and the blood glucose levels are well maintained.

Silvano Piovan, Audrei Pavanello, Giuliana Maria Ledesma Peixoto et al.

Stevia rebaudiana (Bert.) Bertoni besides being a source of noncaloric sweeteners is also an important source of bioactive molecules. Many plant extracts, mostly obtained with ethyl acetate solvent, are rich in polyphenol compounds that present insulinotropic effects. To investigate whether the nonsweetener fraction, which is rich in phenolic compounds isolated from Stevia rebaudiana with the solvent ethyl acetate (EAF), has an insulinotropic effect, including interference at the terminals of the autonomic nervous system of the pancreatic islets of rats. Pancreatic islets were isolated from Wistar rats and incubated with EAF and inhibitory or stimulatory substances of insulin secretion, including cholinergic and adrenergic agonists and antagonists. EAF potentiates glucose-stimulated insulin secretion (GSIS) only in the presence of high glucose and calcium-dependent concentrations. EAF increased muscarinic insulinotropic effects in pancreatic islets, interfering with the muscarinic receptor subfamily M3. Adrenergic inhibitory effects on GSIS were attenuated in the presence of EAF, which interfered with the adrenergic α2 receptor. Results suggest that EAF isolated from stevia leaves is a potential therapy for treating type 2 diabetes mellitus by stimulating insulin secretion only in high glucose concentrations, enhancing parasympathetic signal transduction and inhibiting sympathetic signal transduction in beta cells.

Yu.M. Urmanova, M.S. Saidnazirkhanova

Objective of the study — to investigate the disorders of growth hormone (GH) secretion in women with polycystic ovary syndrome (PCOS) compared to patients with non-functional pituitary adenomas (NFPA). Under our supervision during period from September 2015 to March 2016, there were 15 female outpatients of childbearing age with PCOS and 15 — with NFPA. Average age of patients was 25.5 and 28.9 years, respectively. The duration of disease ranged from 7 months to 9 years. It was found that in both groups, there were neuroendocrine disorders typical for each pathology. So, in the first group of patients with PCOS, the following violations were most often: obesity, striae, acanthosis, аcne, hyperandrogenemia, hyperpolyme­norrhea, and in the second one — secondary amenorrhea, hyperprolactinemia, panhypopituitarism. In both groups, there was anovulation, as well as decline of GH and insulin-like growth factor‑1 (IGF‑1) secretion. In addition, patients with NFPA had significantly decreased basal levels of tropic hormones — GH, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) on the background of hyperprolactinemia and normal values of IGF‑1, while in patients with PCOS, the levels of GH, LH, FSH were reduced on the background of hyperandrogenemia and IGF‑1 decline. Thus, it was found that in the group of patients with PCOS, there was the most significant reduction of basal IGF‑1 levels, whereas GH deficiency was less frequent. Patients with NFPA had panhypopituitarism, namely combined deficiency of GH, LH, FSH, thyroid stimulating hormone, while IGF‑1 deficiency was less frequent. Disorders of GH and IGF‑1 secretion identified in our study confirm the literature data that patients with PCOS have a reduction in the levels of GH and IGF‑1 on the background of hyperinsulinemia and hyperandrogenaemia.

Duo Zhang, Shuang Jiang, Heng Meng

Defective cognitive function is common in patients with diabetes, suggesting that insulin normally exerts anabolic actions in neuron, namely, diabetic encephalopathy. However, because insulin can cross-activate the insulin-like growth factor type 1 receptor (IGF-1R), which also functions in most of tissues, such as muscle and bone, it has been difficult to establish the direct (IGF-1-independent) actions of insulin in the pathogenesis of diabetic encephalopathy. To overcome this problem, we examined insulin signaling and action in primary PC-12 cells engineered for conditional disruption of the IGF-1 receptor (ΔIGF-1R). The results showed that the lower glucose metabolism and high expression of IGF-1R occurred in the brain of the DE rat model. The results also showed the defect of IGF-1R could significantly improve the ability of glucose consumption and enhance sensitivity to insulin-induced IR and Akt phosphorylation in PC12 cells. And meanwhile, IGF-1R allele gene knockout (IGF-1Rneo) mice treated with HFD/STZ had better cognitive abilities than those of wild mice. Those results indicate that insulin exerts direct anabolic actions in neuron-like cells by activation of its cognate receptor and prove that IGF-1R plays an important role in the pathogenesis of diabetic encephalopathy.

O. F Misyura, V. N Shestakov, I. A Zobenko et al.

Цель. Разработка и внедрение технологического процесса кардиореабилитации в условиях специализированного реабилитационного центра.Включение пациентов в программы реабилитации/вторичной профилактики актуально, экономически выгодно и приводит к повышению приверженности дальнейшему лечению. Программы реабилитации, состоящие из оптимальной медикаментозной терапии, достаточной физической активности, коррекции факторов риска и образа жизни, необходимы всем больным, особенно пациентам среднего и высокого риска. Составление программ реабилитации и оценка прогноза их эффективности представляют собой сложную клиническую задачу из-за многочисленности и неоднородности влияющих на их решение факторов.Медицинские технологии направлены на восстановление или улучшение здоровья пациентов с номинальным качеством (достижением желаемого или прогнозируемого результата) и с оптимальными затратами (минимально возможными затратами, не влекущими за собой ухудшения условий труда медперсонала, санитарных и технических норм). Реабилитация кардиологических больных может рассматриваться как технологический процесс, продуктом которого является качество жизни пациентов. Разработанная технология реабилитации предусматривает получение каждым больным необходимого и достаточного объема реабилитационных воздействий в соответствии с едиными стандартами, но с соблюдением персонифицированного подхода. Успех может быть обеспечен только за счет мультидисциплинарного подхода. Основные технологические элементы реабилитации включаются в общую программу одновременно и в тесной взаимосвязи. Они предусматривают проведение риск-стратификации с формированием относительно однородных групп пациентов, коррекцию медикаментозной терапии, выбор программ физической реабилитации, коррекцию образа жизни и факторов риска, использование методов психотерапии и физиотерапии, информационно-образовательную поддержку.Представленная нами концепция модульного построения персонифицированных реабилитационных программ позволяет адаптировать стандартизованную программу реабилитации к индивидуальным особенностям каждого пациента. Построение персонифицированных модульных программ проводится с помощью компьютерных технологий. Каждый программный модуль оформляется стандартно по отношению к общепринятым медицинским рекомендациям и объединяется с другими элементами программы. Поскольку программный модуль представляет собой функционально законченный фрагмент программы, его можно использовать при составлении индивидуальных программ.Заключение. В целом применяемая в реабилитационном центре «Черная речка» технологическая схема кардиореабилитации позволила повысить эффективность реабилитации, в частности, сделать процесс лечения более полно соответствующим установленным стандартам, а труд врача - более осмысленным и результативным.

Feng Xu, Yuehui Wang, Wenpeng Cui et al.

The present study was to investigate the protection of resveratrol (RSV) in diabetes associated with kidney inflammation and cell proliferation. Rat mesangial cell and streptozotocin-induced type 1 diabetes mouse model were used. In vitro, RSV attenuated high glucose-induced plasminogen activator inhibitor (PAI-1) expression and mesangial cell proliferation, as well as Akt and nuclear factor-kappa B (NF-κB) activation. The similar results were recaptured in the experiment with Akt inhibitors. In vivo, mice were divided into three groups: control group, diabetes mellitus (DM) group, and RSV-treated DM group. Compared with control group, the kidney weight to body weight ratio and albumin to creatinine ratio were increased in DM group, but not in RSV-treated DM group. Furthermore, the increased expression of PAI-1 and intercellular adhesion molecule-1 in diabetic renal cortex were also reduced by RSV administration. Besides, the kidney p-Akt/Akt ratio and NF-κB were significantly increased in DM group; however, these changes were reversed in RSV-treated DM group. Additionally, immunohistochemistry results indicated that RSV treatment reduced the density of proliferating cell nuclear antigen-positive cells significantly in glomeruli of diabetic mice. These results suggest that RSV prevents diabetes-induced renal inflammation and mesangial cell proliferation possibly through Akt/NF-κB pathway inhibition.