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Hair loss is a common clinical condition connected with serious psychological distress and reduced quality of life. Hormones play an essential role in the regulation of the hair growth cycle. This review focuses on the hormonal background of hair loss, including pathophysiology, underlying endocrine disorders, and possible treatment options for alopecia. In particular, the role of androgens, including dihydrotestosterone (DHT), testosterone (T), androstenedione (A4), dehydroepiandrosterone (DHEA), and its sulfate (DHEAS), has been studied in the context of androgenetic alopecia. Androgen excess may cause miniaturization of hair follicles (HFs) in the scalp. Moreover, hair loss may occur in the case of estrogen deficiency, appearing naturally during menopause. Also, thyroid hormones and thyroid dysfunctions are linked with the most common types of alopecia, including telogen effluvium (TE), alopecia areata (AA), and androgenetic alopecia. Particular emphasis is placed on the role of the hypothalamic–pituitary–adrenal axis hormones (corticotropin-releasing hormone, adrenocorticotropic hormone (ACTH), cortisol) in stress-induced alopecia. This article also briefly discusses hormonal therapies, including 5-alpha-reductase inhibitors (finasteride, dutasteride), spironolactone, bicalutamide, estrogens, and others. [ABSTRACT FROM AUTHOR]

Copyright of Paediatrics & Family Medicine / Pediatria i Medycyna Rodzinna is the property of Medical Communications Sp. z o.o. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Recent studies suggest that the content of immune components in milk is influenced by the mother's health and also by the infant she feeds. We aimed to evaluate the effect of a child's respiratory tract infection on the cellular composition of breast milk (neutrophils, monocytes, eosinophils, lymphocytes, and their subpopulations). Twenty-six breastfeeding mothers whose children were hospitalized for respiratory tract infections were enrolled in the study. The control group consisted of 23 mothers of healthy children. Regarding the children, baseline laboratory blood tests were performed, and nasal swabs were taken for the presence of RS virus. In the next step, milk samples were collected from the mothers to assess the cellular composition of the milk, including neutrophils, monocytes, eosinophils, lymphocytes, and their subpopulations. Significantly higher percentages of T lymphocytes (helper and cytotoxic lymphocytes) were observed in the milk of the studied mothers. There was a significantly higher percentage of milk lymphocytes in the group of affected children with confirmed RSV etiology than in children with excluded RSV etiology. A significant positive correlation was observed between the duration of infection and the percentage of milk NK cells and between milk CD19 lymphocytes and the child's serum leukocytosis. This study may provide evidence of a link between cells in breast milk and disease in the breastfed infant. The severity of the infection, its duration, and the etiological agent of the infection may affect the cellular composition of milk. [ABSTRACT FROM AUTHOR]

Copyright of Paediatrics & Family Medicine / Pediatria i Medycyna Rodzinna is the property of Medical Communications Sp. z o.o. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Paediatrics & Family Medicine / Pediatria i Medycyna Rodzinna is the property of Medical Communications Sp. z o.o. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Bioactive calcium phosphate ceramics (CaPs) are one of the building components of the inorganic part of bones. Synthetic CaPs are frequently used as materials for filling bone defects in the form of pastes or composites; however, their porous structure allows modification with active substances and, thus, subsequent use as a drug carrier for the controlled release of active substances. In this study, four different ceramic powders were compared: commercial hydroxyapatite (HA), TCP, brushite, as well as HA obtained by wet precipitation methods. The ceramic powders were subjected to physicochemical analysis, including FTIR, XRD, and determination of Ca/P molar ratio or porosity. These techniques confirmed that the materials were phase-pure, and the molar ratios of calcium and phosphorus elements were in accordance with the literature. This confirmed the validity of the selected synthesis methods. CaPs were then modified with the antibiotic clindamycin. Drug release was determined on HPLC, and antimicrobial properties were tested against Staphylococcus aureus. The specific surface area of the ceramic has been demonstrated to be a factor in drug release efficiency. [ABSTRACT FROM AUTHOR]

Copyright of Paediatrics & Family Medicine / Pediatria i Medycyna Rodzinna is the property of Medical Communications Sp. z o.o. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Paediatrics & Family Medicine / Pediatria i Medycyna Rodzinna is the property of Medical Communications Sp. z o.o. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Molecular mimicry between Helicobacter pylori (Hp) and the host components resulting in induction of cross-reacting antibodies has been suggested as accessory mechanism in the development of coronary heart disease (CHD). A potential target for antibodies induced during Hp infection by the components of these bacteria might be amino acid sequence TVLLPVIFF (P1) of tumor necrosis factor receptor (TNFR), which is exposed on vascular endothelium and immunocompetent cells, driving inflammation. Aim: To examine whether anti-P1 IgG are induced during Hp infection in CHD patients. Methods: Sera from CHD patients infected with Hp (54) vs. sera of uninfected healthy donors (22) were tested by the ELISA for anti-H. pylori antibodies, anti-P1 IgG, and for antibodies towards control sequence IAKEGFEKIS (P2). Sera of Caviae porcellus infected experimentally with Hp (30) or uninfected (10) were included into this study. The same serum samples, which were positive for anti-P1 IgG, were adsorbed with Hp and then subjected to the ELISA. The biological activity of anti-P1 IgG was assessed in complement (C1q) binding assay. Results: Sera of 43 CHD patients seropositive for anti-Hp IgG contained anti-P1 IgG binding C1q. Additionally, 10 serum samples of animals seropositive for anti-Hp IgG contained anti-P1 IgG. Anti-P1 IgG in tested sera were neutralized by their adsorption with Hp. Conclusion: In CHD patients infected with Hp, antibodies cross-reacting with TNFR common sequence are produced. Further studies are necessary to define immunogenic Hp determinants and to confirm possible cellular effects of cross-reacting antibodies. [ABSTRACT FROM AUTHOR]

Vitamin D is a hormone regulating the immune system and playing a pivotal role in responses to microbial infections. It regulates inflammatory processes by influencing the transcription of immune-response genes in macrophages, T cells, and dendritic cells. The proven role of vitamin D in many infectious diseases of the respiratory tract indicated that vitamin D should also play a role in SARS-CoV-2 infection. Vitamin D inhibits cytokine storm by switching the pro-inflammatory Th1 and Th17 to the anti-inflammatory Th2 and Treg response. Vitamin D is therefore expected to play a role in preventing, relieving symptoms, or treating SARS-CoV-2 infection symptoms, including severe pneumonia. There are several possible mechanisms by which vitamin D may reduce the risk of COVID-19 infection, such as induction of the transcription of cathelicidin and defensin. Also a nongenomic antiviral action of vitamin D and lumisterol, the molecule closely related to vitamin D, was reported. Despite this enormous progress, currently, there is still insufficient scientific evidence to support the claim that vitamin D supplementation may help treat COVID-19 infection. The pandemic restrictions were also shown to impact vitamin D uptake by limiting exposure to sunlight. [ABSTRACT FROM AUTHOR]

Copyright of Paediatrics & Family Medicine / Pediatria i Medycyna Rodzinna is the property of Medical Communications Sp. z o.o. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Paediatrics & Family Medicine / Pediatria i Medycyna Rodzinna is the property of Medical Communications Sp. z o.o. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Paediatrics & Family Medicine / Pediatria i Medycyna Rodzinna is the property of Medical Communications Sp. z o.o. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Infections with oncogenic human papillomavirus (HPV) strains are recognized as the major risk factor for developing malignant lesions in the uterine cervix. However, several findings have demonstrated cooperation between HPV infection and 17β-estradiol (E2) in cervical carcinogenesis. The 17β-hydroxysteroid dehydrogenase type 1 (HSD17B1) is the enzyme involved in the transformation of estrone (E1) into E2. In this study, we identified the HSD17B1 transcript and protein in HeLa, SiHa, Ca Ski and C-33A cervical cancer cells. These cells were able to convert E1 to E2 in a time-dependent manner. Moreover, we identified the HSD17B1 transcript and protein in primary cancerous tissues ( n = 28) and in histologically unchanged tissues ( n = 25). We did not observe significant differences ( P = 0.33) between the HSD17B1 transcript levels in cancerous tissues and histologically unchanged tissues. However, we found an overrepresentation of the HSD17B1 protein in cancerous tissues compared with histologically unchanged tissues ( P < 0.001). This overrepresentation of the HSD17B1 protein in primary cervical cancerous tissues may be responsible for the local conversion of E1 to E2. [ABSTRACT FROM AUTHOR]

Wstęp: Miażdżyca jest jedną z najczęstszych chorób cywilizacyjnych XXI wieku. Jednym z ważniejszych czynników ryzyka rozwoju miażdżycy jest stan zapalny w obrębie śródbłonka naczyniowego oraz zaburzenia metabolizmu lipidów rozwijające się w organizmie. Ostatnio coraz częściej sugerowany jest udział czynników zakaźnych wywołujących przewlekły stan zapalny organizmu w progresji wczesnych zmian promiażdżycowych. Do wczesnych zmian promiażdżycowych zaliczane są między innymi: nasilenie stresu oksydacyjnego w śródbłonku naczyniowym prowadzące do peroksydacji lipidów, transformacja makrofagów do komórek piankowatych, będących głównym składnikiem blaszek miażdżycowych, oraz niealkoholowe stłuszczenie wątroby. Cel: Charakterystyka wczesnych zmian promiażdżycowych indukowanych w obszarze śródbłonka naczyniowego przez komponenty bakteryjne H. pylori. Materiały i Metody: Do badań wykorzystano dwie linie komórkowe: HMEC-1 (ludzkie komórki śródbłonka naczyniowego) oraz THP1 (monocyty ludzkie). Komórki HMEC-1 eksponowano na działanie lipopolisacharydu H. pylori i 7-ketocholesterolu, a następnie oceniano pod kątem obecności stresu oksydacyjnego. Monocyty ludzkie przekształcono w makrofagi przy pomocy PMA i stymulowano analogicznie do komórek HMEC-1. Następnie w celu określenia odsetka powstałych komórek piankowatych, komórki wybarwiano przy pomocy hematoksyliny oraz czerwieni oleistej i obrazowano w mikroskopie świetlnym. Dodatkowo w badaniach wykorzystano fragmenty aort oraz wątroby pochodzące od kawii domowych zakażonych H. pylori karmionych paszą normalną lub wysokotłuszczową. Skrawki aorty po barwieniu immunohistochemicznym oceniono pod względem obecności stresu oksydacyjnego, a wątroby po wybarwieniu hematoksyliną i eozyną ocenione zostały pod kątem występowania oznak stłuszczenia wątroby. Wyniki: Przeprowadzone badania wykazały wzrost stresu oksydacyjnego w komórkach śródbłonka naczyniowego w odpowiedzi na stymulację lipopolisacharydem H. pylori oraz 7-ketocholesterolem. Barwienie wykonane ex vivo na skrawkach tkanki aortalnej kawii domowych potwierdziło te obserwacje, wskazując na występowanie najsilniejszego stresu oksydacyjnego u zwierząt zakażonych H. pylori karmionych paszą wysokotłuszczową. Dodatkowo komponenty H. pylori w połączeniu z 7-ketocholesterolem silnie stymulowały makrofagi do transformacji w komórki piankowate. Ocena histopatologiczna tkanek wątroby zwierząt wykazała stłuszczenie w większości wielkokropelkowe występujące wokół naczyń u zakażonych H. pylori zwierząt eksponowanych na dietę wysokotłuszczową. Podsumowanie: Śródbłonek naczyniowy eksponowany na LPS H. pylori oraz oksydowane sterole rozwija silny stres oksydacyjny prowadzący do rozwoju wczesnych zmian promiażdżycowych. Co więcej nasilenie transformacji makrofagów w komórki piankowate indukowany czynnikami bakteryjnymi H. pylori intensyfikuje rozrost blaszki miażdżycowej. [ABSTRACT FROM AUTHOR]

Background: The main source of vitamin D is skin synthesis, which depends on sunlight exposure. During the pandemic, COVID-19 children were obliged to home confinement, which potentially limiting sunlight exposure. The aim of this study was to evaluate whether home confinement led to decreased vitamin D serum levels in children in Warsaw, Poland. Methods: The study included 1472 children who were divided into two groups, based on the date of 25(OH)D level blood sampling: before and during the pandemic. Children under 1 year of age (infants) were analysed separately. Results: A statistically significant decrease in the average level of vitamin D was observed between groups of children over 1 year of age (35 ng/mL ± 18 vs. 31 ng/mL ± 14). In infants from both groups, the mean vitamin D levels were within the normal range (Group 1 inf 54 ng/mL ± 21 vs. Group 2 inf 47 ng/mL ± 15). The characteristic seasonal variability was observed before the pandemic, with maximal vitamin D levels in summer (40 ng/mL ± 17) and minimal levels in winter (30 ng/mL ± 14). During the pandemic, no seasonal variability was observed (summer 30 ng/mL ± 11 vs. winter 30 ng/mL ± 19). Conclusions: The COVID-19 pandemic restrictions led to a significant decrease in vitamin D serum levels in children. [ABSTRACT FROM AUTHOR]

Background: Lipopolysaccharide (LPS) of Helicobacter pylori (Hp) bacteria causes disintegration of gastric tissue cells in vitro. It has been suggested that interleukin (IL)-33 is involved in healing gastric injury. Aim: To elucidate whether Hp LPS affects regeneration of gastric barrier initiated by IL-33. Methods: Primary gastric epithelial cells or fibroblasts from Caviae porcellus were transfected with siRNA IL-33. Such cells, not exposed or treated with LPS Hp, were sub-cultured in the medium with or without exogenous IL-33. Then cell migration was assessed in conjunction with oxidative stress and apoptosis, activation of extracellular signal-regulated kinase (Erk), production of collagen I and soluble ST2 (IL-33 decoy). Results: Control cells not treated with LPS Hp migrated in the presence of IL-33. The pro-regenerative activity of IL-33 was related to stimulation of cells to collagen I production. Wound healing by cells exposed to LPS Hp was inhibited even in the presence of IL-33. This could be due to increased oxidative stress and apoptosis in conjunction with Erk activation, sST2 elevation and modulation of collagen I production. Conclusions: The recovery of gastric barrier cells during Hp infection potentially can be affected due to downregulation of pro-regenerative activity of IL-33 by LPS Hp. [ABSTRACT FROM AUTHOR]

In the course of atopic dermatitis (AD), the overactivity of the immune system, associated with predominant Th2 lymphocyte responses, is observed, which leads to an increased inflammatory reaction. Cases of a severe course of atopic dermatitis lead to the search for new therapeutic options. The aim of this study was to assess the effects of hyperbaric oxygen therapy (HBOT) treatment for severe cases of AD in children. A total of 15 children with severe AD underwent therapy. The influence of HBOT on the clinical course of AD and immunomodulatory effect of the therapy was analyzed by the SCORAD and objective SCORAD (oSCORAD) scales and by determining the serum concentration of immunological parameters (blood: nTreg lymphocytes, CD4+CD25highCD127-FOXP3+, NKT lymphocytes CD3+, CD16/56+, and serum: total IgE, cytokines IL-4, IL-6, and IL-10, before and after the 30-day treatment cycle). The study showed a significant effect of the therapy on the improvement of the skin condition. In all children, a reduction in the extent and intensity of skin lesions, reduction of redness, swelling, oozing/crusting, scratch marks and skin lichenification after HBOT was observed. Patients also reported a reduction in the intensity of pruritus and an improvement in sleep quality after therapy. In all children, a statistically significant decrease in the serum level of IgE was observed. However, no statistically significant changes in the blood levels of IL-4, IL-6 and IL-10, as well as the percentage of CD4+CD25highCD127−FOXP3+ Treg and NKT lymphocytes, were found. In conclusion, the use of hyperbaric therapy has a positive impact on treatment results in children with a severe course of atopic dermatitis. [ABSTRACT FROM AUTHOR]

Vitamin D, in addition to its superior role as a factor regulating calcium-phosphate metabolism, shows wide effects in other processes in the human body, including key functions of the immune system. This is due to the presence of vitamin D receptors in most cells of the human body. In our study, we aimed to assess whether there is a correlation between vitamin D content and the clinical course of allergic diseases as well as establish their immunological parameters in children. We found that vitamin D deficiency was significantly more frequent in the group of children with an allergic disease than in the control group (p = 0.007). Statistically significant higher vitamin D concentrations in blood were observed in the group of children with a mild course of the disease compared to children with a severe clinical course (p = 0.03). In the group of children with vitamin D deficiency, statistically significant lower percentages of NKT lymphocytes and T-regulatory lymphocytes were detected compared to the group of children without deficiency (respectively, p = 0.02 and p = 0.05), which highlights a potential weakness of the immune system in these patients. Furthermore, statistically higher levels of interleukin-22 were observed in the group of children with vitamin D deficiency (p = 0.01), suggesting a proinflammatory alert state. In conclusion, these results confirm the positive relationship between the optimal content of vitamin D and the lesser severity of allergic diseases in children, establishing weak points in the immune system caused by vitamin D deficiency in children. [ABSTRACT FROM AUTHOR]