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In this study, it was aimed to investigate the effects of fabric lamination angle and fabric ply number on electromagnetic shielding effectiveness (EMSE) of weft knitted fabric-reinforced polypropylene composites. Knitted fabric-reinforced composites are composed of aramid yarn, polypropylene yarn, and copper wire. Polypropylene is the matrix phase and the aramid yarn and copper wires are the reinforcement phase of the composite materials. It was achieved to form 1.5 to 3 mm thickness composites. The composites have nearly 20–50 dB electromagnetic shielding values. To form the knitted fabrics, 7G semiautomatic flat knitting machine was used. The composites were formed by a laboratory-type hot press. EMSE of composites were tested by using ASTM D 4935 coaxial test fixture in 27–3000 MHz frequency band. Lamination angle and ply number parameters were examined related to EMSE of structures. For this study, three different structures were knitted and named as plain knit, 1×1 rib knit, and half cardigan knit. To determine the effect of lamination angle of composites on electromagnetic shielding performance, the composites were produced in two different lamination angles as 0°/90°/0°/90° and 0°/45°/0°/45°. To determine the effect of fabric ply number of composites on electromagnetic shielding performance, the composites were produced in two and four plies. It was observed that the fabric ply number and lamination angle does not affect the EMSE of composite materials very much. It was determined that weft knitted reinforced composite structures have appropriate and high EMSE values for electromagnetic applications. This knitted fabric-reinforced polypropylene composites are flexible and suitable for other industrial applications as civil engineering, aerospace, etc.

Nonylphenol (NP) is an organic pollutant and endocrine disruptor chemical that has harmful effects on the environment and living organisms. This study looked at whether kidney tissues subjected to increasing doses of nonylphenol generated alterations in histopathologic, pro-inflammatory, and autophagic markers. Fifty rats were divided into five groups of ten each: group I: healthy group, II: control (corn oil), group III: 25 μl/kg NP, group IV: 50 μl/kg NP, group V: 75 μl/kg NP. The kidney tissue samples were obtained for histopathological, immunohistochemical, and biochemical analyses. The histological deteriorations observed in all NP groups included tubular epithelial cell degeneration, inflammation areas, and hemorrhage. The immunohistochemical investigations showed that NP significantly elevated the autophagy markers (Beclin-1, LC3A/B, p62), pro-inflammatory cytokines (TNF-α, IL-6), HIF-1α, and eNOS in group III, IV and V compared with group I and II. The biochemical analysis also revealed that pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) increased in correlation with the NP doses, but only IL-1β reached statistical significance in NP treated rats kidney tissue. The biochemical findings have been confirmed by the histological studies. The damage to renal tissue caused by NP exposure may worsen it by increasing inflammatory and autophagic markers.

Ovarian ischemia is a gynecological emergency that occurs as a result of ovarian torsion, affects women of reproductive age, and reduces ovarian reserve. The current study was designed to investigate the effect of boric acid taken in different ways on histopathological changes, autophagy, oxidative stress, and DNA damage caused by ischemia and reperfusion in the ovary of adult female rats. We established seven groups of 70 adult female rats: untreated control, intraperitoneal boric acid group (IpBA), oral boric acid group (OBA), ischemia/reperfusion group (ischemia/2 h reperfusion; OIR), ischemia/reperfusion and local boric acid group (OIR + LBA), ischemia/reperfusion and intraperitoneal boric acid group (OIR + IpBA), and ischemia/reperfusion and oral boric acid group (OIR + OBA). On the 31st day of the experimental procedure, both ovaries were harvested for histologic (hematoxylen and eosin and Masson trichrom), biochemical (ELISA and AMH, MDA, SOD, and CAT analyses), and comet evaluation. In the OIR group, hemorrhage, edema, inflammation, and diminished follicle reserve were seen in the ovary. Boric acid treatment reduced the ovarian ischemia/reperfusion damage, and the follicles exhibited similar morphological features to the control group. Moreover, boric acid treatment decreased the levels of Hsp70, NF-KB, COX-2, and CD31, which increased as a result of OIR. On the other hand, SCF and AMH levels, which decreased as a result of OIR, increased with boric acid treatment. The levels of autophagy markers (Beclin-1, LC3, and p62) reached values close to those of the control group. According to the biochemical findings, it was concluded that boric acid is also effective on oxidative stress, and the AMH level was particularly high in the OIR + OBA group, consistent with the immunohistochemical staining result. In addition, it was observed that the DNA damage caused by OIR reached values close to those of the control group, especially in the OBA after OIR. This study showed the therapeutic effects of boric acid on OIR injuries; thus, boric acid may be a potential therapeutic agent for ovarian protection and fertility preservation in cases that may cause ovarian torsion., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Obstacles to the successful treatment of breast cancer patients with chemotherapeutic agents can be overcome with effective new strategies. It is still unclear how folic acid affects the onset and spread of breast cancer. The purpose of this study was to determine how folic acid affected the apoptotic and autophagic pathways of the breast cancer cell lines MCF-7 and MDA-MB-231. In the present study, folic acid was applied to MCF-7 and MDA-MB-231 breast cancer cell lines at different concentrations and for different durations. MTT analysis was used to investigate cytotoxic activity. All groups underwent the Tunel staining procedure to identify apoptosis and the immunofluorescence staining approach to identify the autophagic pathway. 24-hour folic acid values were accepted as the most appropriate cytotoxic dose. In MCF-7, cell cycle arrest was observed in the S phase and MDA-MB-231 G1/G0 phases. When apoptotic TUNEL staining was evaluated in both cell lines, folic acid significantly increased apoptosis. While a significant difference was observed between the groups in terms of Beclin 1 immunoreactivity in the MDA-MB-231 cell line, there was no significant difference in the MCF-7 cell line. In addition, statistical significance was not observed LC3 immunoreactivity in both cell lines. In the study, it was observed that folic acid induced autophagy at the initial stage in the MDA-MB-231 cell line but had no inductive effect in the MCF-7 cell line. In conclusion, our findings showed that folic acid has a potential cytotoxic and therapeutic effect on MCF-7 and MDA-MB-231 breast cancer cell lines., (© 2023 Société Française de Pharmacologie et de Thérapeutique. Published by John Wiley & Sons Ltd.)

In this study, we reported boric acid's protective effects on the quality of nonylphenol (NP)-exposed oocytes. Female rats were classified into 4 groups: control, boric acid, NP, and NP+boric acid. Histopathological studies and immunohistochemical analysis of anti-müllerian hormone (AMH), mechanistic target of rapamycin (mTOR), Sirtuin1 (SIRT1), stem cell factor (SCF) studies were done. The comet assay technique was utilized for DNA damage. The ELISA method was used to determine the concentrations of oxidative stress indicators (SOD, CAT, and MDA), ovarian hormone (INH-B), and inflammation indicators (IL-6 and TNF-α). Boric acid significantly reduced the histopathological alterations and nearly preserved the ovarian reserve. With the restoration of AMH and SCF, boric acid significantly improved the ovarian injury. It downregulated SIRT1 and upregulated the mTOR signaling pathway. It provided DNA damage protection. Ovarian SOD, CAT levels were decreased by boric acid. Boric acid co-administration significantly reduced NP's MDA, IL-6, and TNF-activities. This results imply that boric acid has a protective role in ovarian tissue against NP-mediated infertility., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Determining the molecular characteristics of the damage caused by NP exposure in the testis is very important for understanding the source of the damage and developing treatment methods accordingly. Therefore, in this study, it is aimed to evaluate the toxic effects that different doses of NP may cause in the testis, including blood-testicular barrier integrity and sperm DNA damage. For this purpose, 50 adult male Wistar albino rats were used in the study. Low, medium, and high-dose NP groups and the corn oil group were formed. After NP administration at determined doses for 15 days, the testis tissue taken under anesthesia was fixed in formaldehyde. Paraffin blocks were embedded using the routine histological tissue follow-up method. Histopathological and immunohistochemical analyses were performed by taking 5 μm thick sections from paraffin blocks. The other testicular tissue was taken for the Western blot, Elisa, and comet methods, and the findings of sperm DNA analysis and the blood-testicular barrier were examined. NP caused the seminiferous epithelium to be disorganized and have significantly fewer cells in the testes of rats in different dose NP-induced groups. Compared with the control group, mTOR, Cx43, SCF, and HSP70 protein levels were decreased, while the expression of MMP-9 levels was increased in the different NP dose groups. Furthermore, tissue testosterone and inhibin B levels and SF-1 immunoreactivity intensity gradually decreased depending on the dose increase of NP. DNA damage of testicular tissues were increased in NP groups depending on NP dose. These results suggest that it is evident that NP, a commonly used industrial chemical, is an endocrine disrupting chemical (EDC) with estrogenic activity exerting adverse effects on health and that urgent measures are needed regarding the use., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

We investigated using histochemistry and immunohistochemistry ovarian damage caused by nonylphenol (NP) and the protective effect of melatonin treatment of NP induced ovarian damage. We used 21 female rats divided randomly into three groups: control, NP and melatonin + NP. Histopathological examination of the ovaries, and counting and classification of follicles were performed using Masson's trichrome staining. Expression of anti-Mullerian hormone (AMH), Bax, Bcl-2 and caspase-3 was detected in the ovaries using immunohistochemistry. Melatonin had an ameliorative effect on NP induced follicular atresia and absence of corpora lutea. More follicles were observed in the ovaries of animals treated with melatonin prior to treatment with NP. AMH immunoreactivity was significantly lower in the NP group than in the melatonin + NP group. NP increased immunostaining for Bax, Bcl-2 and caspase-3. Melatonin significantly reduced the increased expression of Bax, Bcl-2 and caspase-3 due to NP exposure. We found that pretreatment with melatonin is beneficial for protecting the ovaries from damage by NP.

Doxorubicin (DOX) is a widely used drug for the treatment of cancer,but its clinical use is limited by its liver toxicity. Administering DOX with an antioxidant has become a strategy for preventing the side effects of DOX. Although selenium (Se) is an important trace mineral, data concerning the effect of Se on DOX induced liver tissue are lacking. We investigated the mechanism of DOX hepatotoxicity and the protective effect of different doses of Se on Dox induced liver damage. Female Wistar albino rats were divided into eight equal groups. Se was injected intraperitoneally (i.p.) to rats at doses of 0.5, 1, and 2 mg 0.5 h after injection i.p. of 5 mg/kg DOX on days 1, 7, 14, 21 and 28. Liver histopathology was assessed to determine the dose at which Se may best inhibit Dox induced liver toxicity. Also, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) expression levels and proliferating cell nuclear antigen (PCNA) activity were determined using immunohistochemistry. We found that DOX caused liver damage and increased TNF-α, IL-1β and PCNA levels. Se prevented structural damage to liver tissues. Our findings reinforce the protective effects of Se in rat liver.

Background: Investigating the effects of 405-nm, 532-nm, 650-nm, and 950-nm wavelengths of LLLTs (low-level laser therapies) on the orthodontic tooth movement in rats by using histological and immunohistochemical methods. Forty-five Wistar albino rats were randomly divided into 5 groups: control group (positive control: the left maxillary 1st molar side; negative control: the right maxillary 1st molar side), 405 nm LLLT group (Realpoo), 532 nm LLLT group (Realpoo), 650 nm LLLT group (Realpoo), and 940 nm LLLT group (Biolase). The left maxillary 1st molar teeth of all rats were applied mesially 50-g force. Starting from the 1st day, 48 h intervals, LLLT was applied in continuous wave mode and in contact with the tissue. The application area was approximately 1 cm 2 . The lasers were performed for 3 min on each surface (buccal, palatal, mesial), totally 9 min (total dose 54 J/cm 2 ). The amount of the molar mesialization, the bone area between the roots, PDL (periodontal ligament) measurements, TRAP (tartrate-resistant acid phosphatase), and ALP (alkaline phosphatase) immunoreactivity intensity were calculated., Results: The amount of the molar mesialization was significantly higher in the 650 nm LLLT group (mean 0.878 ± 0.201 mm; 95% CI (confidence interval) 0.724 and 1.032) than in the groups of positive control (mean 0.467 ± 0.357 mm; 95% CI 0.192 and 0.741) and 405 nm LLLT (mean 0.644 ± 0.261 mm; 95% CI 0.443 and 0.845) (p < 0.001). There were significant differences in the PDL-mesial (p = 0.042) and PDL-distal (p = 0.007) regions between the groups. The immunoreactivity intensity for TRAP-mesial was significantly higher in the positive control group (mean 109,420.33 ± 8769.17; 95% CI 100,217.65 and 118,623.02) than in the 405 nm (mean 91,678.83 ± 7313.39; 95% CI 84,003.9 and 99,353.77) and the 650 nm LLLT (mean 87,169.17 ± 4934.65; 95% CI 81,990.56 and 92,347.77) groups (p = 0.002). There was no statistically significant difference between the groups on immunoreactivity intensity with ALP staining., Conclusions: The results of this study show that LLLT with 650-nm wavelength increases orthodontic tooth movement more than 405-nm, 532-nm, and 940-nm LLLTs. The 940-nm and 650-nm LLLTs also increase the bone area between the roots by more than 405-nm and 532-nm wavelengths.

Although it is generally regarded appropriate to start chemotherapy promptly after a diagnosis of diffuse large B-cell lymphoma (DLBCL), the optimal time from diagnosis to treatment (TDT) is unknown. A total of 689 patients diagnosed with DLBCL and treated with ≥ 1 cycle of CHOP-R with curative intent during 2003-2008 in British Columbia were identified: 347 (50%) TDT ≤ 4 weeks, 277 (40%) TDT 5-8 weeks, 65 (10%) TDT > 8 weeks. For the respective TDT groups, 5-year OS estimates were 61%, 74%, 63% (p = 0.006); 5-year PFS 57%, 70%, 61% (p = 0.006); and 5-year DSS 64%, 80%, 77% (p <0.001). In multivariate analysis, TDT >8 weeks was associated with worse OS (HR 1.20 (95% CI 1.03, 1.41), p = 0.020), PFS (HR 1.33 (95% CI 1.15, 1.54), p < 0.001), and DSS (HR 1.40 (95% CI 1.10, 1.78), p = 0.006). Clinicians should endeavor to initiate curative chemotherapy as soon as possible after a diagnosis of DLBCL is established.

Background: We examined the relationship between location of residence at the time of diagnosis of diffuse large B-cell lymphoma (DLBCL) and health outcomes in a geographically large Canadian province with publicly funded, universally available medical care., Patients and Methods: The British Columbia Cancer Registry was used to identify all patients 18-80 years of age diagnosed with DLBCL between January 2003 and December 2008. Home and treatment center postal codes were used to determine urban versus rural status and driving distance to access treatment., Results: We identified 1,357 patients. The median age was 64 years (range: 18-80 years), 59% were male, 50% were stage III/IV, 84% received chemotherapy with curative intent, and 32% received radiotherapy. There were 186 (14%) who resided in rural areas, 141 (10%) in small urban areas, 183 (14%) in medium urban areas, and 847 (62%) in large urban areas. Patient and treatment characteristics were similar regardless of location. Five-year overall survival (OS) was 62% for patients in rural areas, 44% in small urban areas, 53% in medium urban areas, and 60% in large urban areas (p = .018). In multivariate analysis, there was no difference in OS between rural and large urban area patients (hazard ratio [HR]: 1.0; 95% confidence interval [CI]: 0.7-1.4), although patients in small urban areas (HR: 1.4; 95% CI: 1.0-2.0) and medium urban areas (HR: 1.4; 95% CI: 1.0-1.9) had worse OS than those in large urban areas., Conclusion: Place of residence at diagnosis is associated with survival of patients with DLBCL in British Columbia, Canada. Rural patients have similar survival to those in large urban areas, whereas patients living in small and medium urban areas experience worse outcomes.

P-cadherin is a calcium-dependent cell-cell adhesion glycoprotein. P-cadherin expression is restricted to the myoepithelial cells in normal breast tissue, and aberrant staining has also been described in invasive tumors. Several small studies have reported P-cadherin as a marker of poor outcome in breast cancer patients but its prognostic significance in relation to other variables has not been established in a large series of breast cancers. A tissue microarray was constructed from 3992 cases of invasive breast carcinoma, and P-cadherin expression was evaluated using immunohistochemistry. Median follow-up was 12.5 years. The immunohistochemistry-based definitions of cancer subtypes were luminal (ER+ or PR+/HER2-), luminal/HER2+ (ER+ or PR+/HER2+), HER2+ (ER-/PR-/HER2+), and basal (ER-/PR-/HER2-/CK5/6+ or EGFR+). Clinical covariate and biomarker associations were assessed using contingency tables, and Pearson's χ(2) or Fisher's exact test. Survival associations were assessed using Kaplan-Meier plots, logrank and Breslow tests, and Cox proportional hazards regression analysis. P-cadherin was expressed in 34.8% (1290/3710, 50% cut point) of cases. P-cadherin staining was strongly associated with HER2+ and basal carcinoma subtypes (P<0.0005). P-cadherin-positive patients showed significantly poorer short-term (0-10 years) overall survival, disease-specific survival, distant relapse-free interval, and locoregional relapse-free interval in univariable models (P<0.05). In multivariable Cox models containing standard clinical covariates and cancer subtypes, P-cadherin did not show independent prognostic value. P-cadherin expression was positively associated with histological grade, chemotherapy, Ki-67, EGFR, CK5/6, p53, YB-1, and HER2 expression (P<0.002), and negatively associated with age at diagnosis, ER, PR, and Bcl-2 expression (P<0.0005). This study shows the value of P-cadherin as a marker of poor prognosis. The large sample size of this series clarifies contradictory findings of many smaller studies. P-cadherin positivity is associated with high-grade tumor subtypes and well-established markers of poor prognosis, and may represent a promising antibody therapeutic target.