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Citalopram is the most potent selective serotonin reuptake inhibitor, commonly prescribed as an antidepressant, which can cause sexual dysfunction. Melatonin is a natural, highly effective antioxidant playing a pivotal role in the male reproductive system. The present study aimed to explore the ameliorating potential of melatonin on citalopram-evoked testicular toxicity and injury in mice. In this regard, mice were randomly divided into six groups: control, citalopram, melatonin 10 mg/kg, melatonin 20 mg/kg, melatonin 10 mg/kg plus citalopram, and melatonin 20 mg/kg plus citalopram. Adult male mice were intraperitoneally (i.p.) injected with 10 mg/kg of citalopram for 35 days with or without melatonin. At the end of the study, sperm parameters, testosterone level, testicular levels of malondialdehyde (MDA), nitric oxide (NO), total antioxidant capacity (TAC), and apoptosis (Tunel essay) were evaluated. Our findings revealed that melatonin restored spermatogenesis by improving sperm count, motility, viability, morphology, and chromatin integrity. Testosterone levels and the histopathology of the testes were markedly improved in the melatonin-administrated groups. Furthermore, citalopram administration significantly increased oxidative stress; however, melatonin restored antioxidant status by enhancing TAC levels and decreasing NO and MAD levels. More notably, citalopram therapy induced a significant increase in the number of Tunel-positive cells, while melatonin administration significantly mitigated the apoptotic impacts of citalopram. Together, melatonin therapy provides protection against citalopram-induced testicular damage via modulating nitro-oxidative stress and apoptosis, which provides evidence for melatonin as a promising treatment against antidepressant drug-associated reproductive toxicity and male sub/infertility. • Melatonin attenuates citalopram-induced testicular toxicity and sperm damage. • Melatonin regulates nitro-oxidative stress and apoptosis in testes. • The beneficial effects of melatonin were not dose-dependent. • Melatonin could alleviate antidepressant-associated reproductive toxicity. [ABSTRACT FROM AUTHOR]

Abstract: In this paper we introduce a new technical development of branching processes that can potentially model spread of epidemics by including various stages of infection. In fact, we present an epidemic model that the disease spreads from an individual to another one in such a way that the ability of individual u to infect a susceptible individual depends only on how long u has been infected. For analysis of this model, we introduce a new and special model of the Crump–Mode–Jagers branching processes in discrete time and obtain some of its fundamental properties. [Copyright &y& Elsevier]

There is growing concern that some cytotoxic regimens for cancer adversely affect spermatogenesis and male fertility. Increasing evidence demonstrated that melatonin has beneficial impacts on reproductive processes; however, whether melatonin can protect against bleomycin, etoposide, and cisplatin (BEP) chemotherapy regimen-induced testicular toxicity, remains obscure. The present study aimed to explore the effect of melatonin on BEP-evoked testicular injury in rats. Adult male Wistar rats (n = 10/group) were intraperitoneally (i.p.) injected with one cycle of 21 days of 0.33 therapeutically relevant dose levels of BEP (.5 mg/kg bleomycin, 5 mg/kg etoposide, and 1 mg/kg cisplatin) with or without melatonin. At the end of the study, sperm parameters, testosterone level, stereology of testes, testicular levels of malondialdehyde (MDA), nitric oxide (NO), and total antioxidant capacity (TAC), the expression of apoptosis-associated genes such as Bcl2 , Bax , Caspase-3 , p53 , and TNF-α (Real-time PCR and Immunohistochemistry) were evaluated. Our findings showed that melatonin restored spermatogenesis by improving sperm count, motility, viability, and morphology. Testosterone level, histopathology, and stereology of testes were significantly improved in melatonin-administrated groups. Furthermore, melatonin recovered the oxidative status of the testes through elevating TAC and ameliorating MDA and NO levels. More importantly, melatonin therapy suppressed BEP-evoked apoptosis by modulating Bcl-2 , Bax , Caspase-3 , p53 , and TNF-α expression in testes. In conclusion, melatonin protects the testes against BEP-induced testicular damage by attenuating nitro-oxidative stress, apoptosis, and inflammation, which provides evidence for melatonin as a possible clinical therapy against BEP-associated gonadotoxicity and male sub/infertility. [Display omitted] • Melatonin attenuated bleomycin, etoposide, and cisplatin (BEP) chemotherapy-induced testicular toxicity. • Melatonin's protective effect was attributed to nitro-oxidative stress, apoptosis, and inflammation regulation. • Melatonin alleviative effects were not exerted in a dose-dependent manner. • Melatonin might be a pharmacological therapeutic approach for minimizing BEP-associated male infertility. [ABSTRACT FROM AUTHOR]

The new (3 + 1)-dimensional generalized Kadomtsev–Petviashvili equation, which was introduced by Wazwaz and El-Tantawy in 2016, has been studied analytically. There are two tools of integration are employed to solve this mathematical–physical model. First, We reported the solitary wave solutions including the dark and singular solitons using the generalized Kudryashov method. Then we obtained the hyperbolic traveling wave solutions, trigonometric traveling wave solutions and rational function solutions with the help of the G ′/ G -expansion method, these solutions can be reduced solitary wave solutions and periodic wave solutions under some particular cases. [ABSTRACT FROM AUTHOR]