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This study investigated the influence of special anchoring holes on the bond-slip behavior between CFRP composites and concrete. For this purpose, one hundred and forty-four concrete prisms (200 × 200 × 200 mm) were casted with different concrete compressive strength (20 MPa, 30 MPa, 40 MPa), holes direction (N: None, V: Vertical (Parallel to the fibers), H: Horizontal (Perpendicular to the fibers)), number of holes (0: None, 1, 2, 3, 4), CFRP sheet bonded length (100 mm, 150 mm) and CFRP sheet bonded width (100 mm, 150 mm). The bonding surface of each concrete blocks was prepared and then anchoring holes were drilled using rotary drill before bonding of CFRP sheet. The experimental results showed that the pattern of the anchoring holes has a significant effect on the bond-slip behavior. In general, both the bond strength and ultimate slippage increase as the number of holes increases and as the CFRP sheet width or length increase. However, for an equivalent CFRP sheet area, the influence of the length (parallel to the direction of loading) is more significant in improving the bond strength than the influence of the width of CFRP sheet. For similar number of anchoring holes, the horizontal (Perpendicular to the fibers) pattern was the most effective followed by vertical (Parallel to the fibers) pattern, and one-hole pattern respectively. The special characteristic of the present study is that the new proposed bond–slip model is based on anchored hole CFRP composite and concrete; instead, the existing bond–slip models are based on CFRP composite without anchorage and ordinary concrete. This proposed model is then assessed using experimental test results on anchored holes concrete bonded blocks subjected to double-shear pull-off test, existing bond–slip models in the literature, and database of pull tests published by several researchers. Finally, the proposed bond–slip model is provided an accurate prediction of the large test database of bond strength and corresponding slippage.

Background: Infectious diseases and vaccines can occasionally cause new-onset or flare of immune-mediated diseases (IMDs). The adjuvanticity of the available SARS-CoV-2 vaccines is based on either TLR-7/8 or TLR-9 agonism, which is distinct from previous vaccines and is a common pathogenic mechanism in IMDs., Methods: We evaluated IMD flares or new disease onset within 28-days of SARS-CoV-2 vaccination at five large tertiary centres in countries with early vaccination adoption, three in Israel, one in UK, and one in USA. We assessed the pattern of disease expression in terms of autoimmune, autoinflammatory, or mixed disease phenotype and organ system affected. We also evaluated outcomes., Findings: 27 cases included 17 flares and 10 new onset IMDs. 23/27 received the BNT - 162b2 vaccine, 2/27 the mRNA-1273 and 2/27 the ChAdOx1 vaccines. The mean age was 54.4 ± 19.2 years and 55% of cases were female. Among the 27 cases, 21 (78%) had at least one underlying autoimmune/rheumatic disease prior the vaccination. Among those patients with a flare or activation, four episodes occurred after receiving the second-dose and in one patient they occurred both after the first and the second-dose. In those patients with a new onset disease, two occurred after the second-dose and in one patient occurred both after the first (new onset) and second-dose (flare). For either dose, IMDs occurred on average 4 days later. Of the cases, 20/27 (75%) were mild to moderate in severity. Over 80% of cases had excellent resolution of inflammatory features, mostly with the use of corticosteroid therapy. Other immune-mediated conditions included idiopathic pericarditis ( n = 2), neurosarcoidosis with small fiber neuropathy ( n = 1), demyelination ( n = 1), and myasthenia gravis ( n = 2). In 22 cases (81.5%), the insurgence of Adverse event following immunization (AEFI)/IMD could not be explained based on the drug received by the patient. In 23 cases (85.2%), AEFI development could not be explained based on the underlying disease/co-morbidities. Only in one case (3.7%), the timing window of the insurgence of the side effect was considered not compatible with the time from vaccine to flare., Interpretation: Despite the high population exposure in the regions served by these centers, IMDs flares or onset temporally-associated with SARS-CoV-2 vaccination appear rare. Most are moderate in severity and responsive to therapy although some severe flares occurred., Funding: none.

Establishment of an in vitro system that allows the development of testicular germ cells to sperm will be valuable for studies of spermatogenesis and future treatments for male infertility. In the present study, we developed in vitro culture conditions using three-dimensional agar culture system (SACS), which has the capacity to induce testicular germ cells to reach the final stages of spermatogenesis, including spermatozoa generation. Seminiferous tubules from testes of 7-day-old mice were enzymatically dissociated, and intratubular cells were cultured in the upper layer of the SACS in RPMI medium supplemented with fetal calf serum (FCS). The lower layer of the SACS contained only RPMI medium supplemented with FCS. Colonies in the upper layer were isolated after 14 and 28 days of culture and were classified according to their size. Immunofluorescence and real-time PCR were used to analyse specific markers expressed in undifferentiated and differentiated spermatogonia (Vasa, Dazl, OCT-4, C-Kit, GFR-α-1, CD9 and α-6-integrin), meiotic cells (LDH, Crem-1 and Boule) and post-meiotic cells (Protamine-1, Acrosin and SP-10). Our results reveal that it is possible to induce mouse testicular pre-meiotic germ cell expansion and induce their differentiation to spermatozoa in SACS. The spermatozoa showed normal morphology and contained acrosomes. Thus, our results demonstrate that SACS could be used as a novel in vitro system for the maturation of pre-meiotic mouse germ cells to post-meiotic stages and morphologically-normal spermatozoa.

Problem: This study examined the effect of intraperitoneal administration of lipopolysaccharide (LPS) to adult male mouse on the expression levels of interleukin-18 (IL-18), IL-18 receptor (IL-18R) and the IL-1beta converting enzyme (ICE) (IL-18 family) in their testes and spleen (control)., Method of Study: Adult mice were injected (intraperitoneally; i.p.) with saline (control) or LPS (2, 20, 100 microg/mL; 100 microL/mouse). After 3 and 24 hr, testes and spleen were collected. Testicular tissue was examined for IL-18 (by ELISA, real time PCR, and western blot analysis), IL-18R and ICE (western blot and real time PCR analysis) and spleen tissue was examined for the IL-18 family by real time PCR analysis. Student's t-test was used for statistical analysis., Results: Homogenates of mouse testes contain and express basal levels of IL-18, ICE and IL-18 R. The expression levels of IL-18, ICE and IL-18R were significantly increased 3 and 24 hr after intraperitoneal injection of LPS to mature mouse, as examined by ELISA, western blot and real time PCR analysis. However, the expression levels of IL-18, ICE and IL-18Ralpha in the spleen increased significantly only after 24 hr of LPS stimulation, as examined by real time PCR., Conclusion: Our results demonstrate that LPS increases the expression levels of the IL-18 family in mouse testis and spleen, but the time of expression differs between the two organs. The presence of IL-18 in the testes might be involved in the regulation of physiological and infection/inflammatory processes, and may be part of the autocrine/paracrine factors that control spermatogenesis. Further studies should be performed to confirm this possibility.

In this study we examined the cellular origin and the expression levels of interleukin-18 (IL-18), IL-18 receptor (IL-18R) and IL-1beta-converting enzyme (ICE), which activates pro-IL-18, during normal maturation of murine testis. The levels of IL-18, IL-18R and ICE were significantly higher in testicular tissues and homogenates (but not in the spleen or liver) from sexually immature than mature mice. Immunohistochemical staining of testicular tissues from sexually immature and mature mice shows that testicular germ cells and Leydig cells/interstitial cells express higher levels of IL-18, as compared to other testicular cells. Peritubular cells of sexually immature and mature mice also expressed IL-18. Our results demonstrate, for the first time, over-expression of the IL-18 family in testicular tissues of sexually immature mice, as compared to mature mice, as well as the expression of IL-18 in the different stages of differentiation of testicular germ cells. Thus, our results may indicate involvement of the endocrine system (gonadotropins and testosterone) in the regulation of the testicular IL-18 family, which could be involved in the regulation of testicular functions, development and spermatogenesis under physiological conditions.

In the present study, we examined the cellular origin and the expression levels of interleukin-18 binding protein (IL-18 BP), during normal maturation of murine testis. Immunohistochemical staining of testicular tissues from sexually mature mice, shows that testicular germ cells, at different stages of differentiation, express IL-18 BP. Leydig cells/interstitial cells and peritubular cells express higher levels of IL-18 BP, as compared to other testicular cells. The levels of IL-18 BP were similar in testicular tissues and homogenates from sexually immature and mature mice, as examined by western blot, ELISA and real time PCR analysis. Our results demonstrate, for the first time, the expression of IL-18 BP in murine testicular tissues and cells. Together with our previous studies, which showed over-expression of IL-18 in testicular tissues of immature mice as compared with mature mice, these results may indicate a role for IL-18 in testicular development, and also in the regulation of testicular functions under physiological conditions.