Background The high prevalence and mortality of coronavirus disease 2019 (COVID-19) have made it the most important health and social challenge around the world. However, this disease can be largely prevented by adherence to hygienic principles and protective behaviors. It seems that identifying the processes involved in protective health behaviors can be effective in planning and implementing suitable interventions to encourage the community toward protective behaviors. Therefore, the present study aimed to predict the preventive behaviors of COVID-19 according to the Protection Motivation Theory (PMT). Methods This cross-sectional study was conducted over 2 months in Hormozgan Province, Iran. The study population consisted of all citizens above the age of 15 years. An online questionnaire was used to collect the data. The questionnaire link was available to the participants through social networks. The questionnaire consisted of two sections, including the demographic information and the PMT constructs. All statistical calculations and hypothesis testing were performed in SPSS Version 21 and AMOS Version 21. The significance level was considered to be 0.05 for hypothesis testing. Results A total of 2032 subjects, with the mean age of 34.84 ± 9.8 years (r = 15–98), participated in this study. Most of the participants were 31–40 years old, female (60.4%), married (72%), urban residents (87.3%), and employed (58.8%). The majority of them also had a bachelor’s degree or higher (58.8%). Significant positive correlations were observed between the preventive behaviors of COVID-19 and the perceived vulnerability (r = 0.192, P < 0.001), perceived severity (r = 0.092, P < 0.001), response efficacy (r = 0.398, P < 0.001), self-efficacy (r = 0.497, P < 0.001), and protection motivation (r = 0.595, P < 0.001). On the other hand, significant negative correlations were found between the preventive behaviors of COVID-19 and maladaptive behavior rewards (r = − 0.243, P < 0.001) and perceived costs (r = − 0.121, P < 0.001). Conclusion The present findings showed that maladaptive behavior reward and fear negatively predicted the protective behaviors. On the other hand, response efficacy and self-efficacy positively predicted the protective behaviors; the impact of self-efficacy was the strongest. Overall, the information provided in this study can contribute to health policymaking in Iran.

Laying hens were killed at hourly intervals during the 26-h laying cycle. The 3 largest follicles of the size hierarchy were removed and plasma samples were obtained from the same hens. The follicle walls and the plasma were assayed by RIA for estrogen (E), progesterone (P4), and testosterone (T). The data show that for E and T there is an inverse relationship between follicle size and hormone concentration. There is no such difference for P4. Both E and T show a significant drop immediately after ovulation; P4 does not. Both T and E concentrations rise significantly and synchronously at about 4 and at 8 h after ovulation. The OAAD assay of plasma shows a peak of LH about that time. P4 does not show such a rise in concentration. About 8 to 10 h prior to the next ovulation T concentration in all 3 follicles begins to rise, P4 rises only in the largest follicle and E only in the smallest. All three steroids reach highly significant peaks about 4 to 6 h prior to the next ovulation. Both OAAD and RIA detect plasma LH peaks at about that time. Plasma E and follicle E peak synchronously at 4 to 8 h; T peaks occur at 10 to 12 h after ovulation and are asynchronous with the T follicle peaks. All 3 steroids begin to rise in the plasma about 10 h prior to the next ovulation and all 3 peak together about 4 to 5 h prior to ovulation. The present data do not allow to distinguish between rates of steroid synthesis and their release into the plasma. Whether the steroid peaks occurring in both follicles and plasma shortly before the next ovulation are caused by LH or are the cause of its release remains to be determined.

The possibility that GnRH or a GnRH-like material of ovarian origin may play a physiological role in follicular development was explored in immature hypophysectomized rats by testing whether a potent synthetic antagonist of GnRH action [( N-acetyl-dehydro-Pro1,D-p-chloro-Phe2,D-Trp3,6]GnRH), would potentiate FSH-induced maturation of ovarian follicles to an ovulable stage. Rats were hypophysectomized on day 25 of their life and implanted with a Silastic capsule containing diethylstilbestrol. On day 30, they were started on injections of 10 micrograms NIH FSH-S12 twice daily alone (control) or in combination with 10 micrograms of either native GnRH or GnRH antagonist. On day 35, all rats received 30 IU hCG to trigger ovulation and luteinization of mature follicles. Rats were killed 25.5-28 h later and inspected for number of ova in Fallopian tubes, ovarian weight, number of corpora lutea (CL) on ovarian surface, and appearance of hematoxylin-eosin-stained ovarian slices. In control animals (n = 6), we found some ovulations (mean +/- SEM, 3.2 +/- 1.1/rat), many more CL (16.5 +/- 4.5/rat), and ovarian weights of 37.7 +/- 1.1 mg/rat. In GnRH-treated rats (n = 5), there were no CL formed, no ova were found, and ovarian weights were 16.0 +/- 1.5 mg/rat. In contrast, in GnRH antagonist-treated rats (n = 5), 16.4 +/- 1.6 ova/rat were recovered from the Fallopian tubes, and ovaries contained 20.8 +/- 2.5 CL/rat and weighed 52.7 +/- 3.2 mg/rat. All changes were statistically significant. We conclude that an antagonist of GnRH action is able to potentiate the action of FSH on ovarian follicle development and suggest that it does so by inhibiting the action of an endogenous GnRH or GnRH-like substance that may play a role as a physiological atretic signal.

The δ opioid receptors (DORs) modulate T cell proliferation, IL-2 production, chemotaxis, and intracellular signaling. Moreover, in DOR-transfected Jurkat cells, δ opioids have been shown to suppress HIV-1 p24 Ag expression. These observations led us to characterize the expression of DORs by human peripheral blood T cells and to determine whether a specific DOR agonist, benzamide,4-{[2,5-dimethyl-4-(2-propenyl)-1-piperazinyl](3-methoxyphenyl)methyl]-N,−,{2S[1(S*),2α,5β]}-(9Cl) (SNC-80), can suppress p24 Ag expression by HIV-1-infected CD4+ T cells obtained from normal donors. By immunofluorescence flow cytometry, PHA stimulated the expression of DOR from 1.94 ± 0.70 (mean ± SEM) to 20.70 ± 1.88% of the PBMC population by 48 h (p &lt; 0.0001). DOR expression was ∼40% of both the PHA-stimulated CD4+ and CD8+ T cell subsets, and virtually all DORs were found on these subsets. To determine whether activated DORs suppress HIV-1 expression, PBMC were prestimulated with PHA, and then CD4+ T cells were purified, pretreated with SNC-80, and infected with HIV-1. In a concentration-dependent manner, SNC-80 inhibited production of p24 Ag. SNC-80 10−10 M maximally suppressed (∼50%) both lymphocytotropic (HIV-1 MN) and monocytotropic (SF162) strains; higher concentrations were less effective. Naltrindole, a selective DOR antagonist, abolished the inhibitory effects of SNC-80. Kinetic studies indicated that 24-h pre- or postincubation with SNC-80, relative to infection with HIV-1, eliminated its suppressive effects. Thus, stimulating the DORs expressed by activated CD4+ T cells significantly suppressed the expression of HIV-1. These findings suggest that opioid immunomodulation directed at host T cells may be adjunctive to standard antiviral approaches to HIV-1 infection.