Association between the Treatment of Rosacea and Eradication of Helicobacter Pylori Infection.

Background: Rosacea is a multifactorial skin inflammatory disorder with an unknown cure. Genetics and environmental factors such as microorganisms are involved in the rosacea etiology, for example, Helicobacter pylori have been suggested in rosacea progression. The present study investigated the relationship between H. pylori eradication and rosacea patient's improvement. Materials and Methods: H. pylori infection was investigated in 60 rosacea patients and 65 sex- and age-matched healthy control through enzyme-linked immunosorbent assay (ELISA) and HpSag tests. After infection confirmation, randomly half of the rosacea patients were treated for H. pylori eradication (test), and others received standard treatment (control). HpSag and ELISA tests were repeated after infection eradication and disease flow was surveyed for 60 days. The groups were compared using the ANOVA (Analysis Of Variance) test at the significant level of P < 0.05. Results: At the baseline, the mean of immunoglobulin G (IgG) (59.27 ± 41.4 RU/mL) and immunoglobulin M (IgM) (11.55 ± 6.1 RU/mL) in rosacea patients was higher than the level of IgG (41.38 ± 54.33 RU/mL) and IgM (8.11 ± 8.91 RU/mL) in healthy control (P < 0.04) and (P < 0.01), respectively. Also, the values for H. pylori infection were positive in all patients and 10 healthy controls. The mean titer of IgM and IgG in the test and control patients groups were different at baseline and after treatment. Furthermore, in the test patients group, the mean of IgG was reduced in active rosacea after treatment, and 63.9% of active patients showed rosacea remission after H. pylori eradication. Conclusion: Data suggest the exacerbating role of H. pylori in rosacea, and its eradication along with other therapeutic methods causes rosacea improvement.

Role of genetic variants and host polymorphisms on COVID-19: From viral entrance mechanisms to immunological reactions.

Coronavirus disease 2019 (COVID-19), caused by a highly pathogenic emerging virus, is called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Knowledge regarding the pathogenesis of this virus is in infancy; however, investigation on the pathogenic mechanisms of the SARS-CoV-2 is underway. In COVID-19, one of the most remarkable characteristics is the wide range of disease manifestation and severity seen across individuals of different ethnic backgrounds and geographical locations. To effectively manage COVID-19 in the populations, beyond SARS-CoV-2 detection, serological response assessment, and analytic techniques, it is critical to obtain knowledge about at-risk individuals and comprehend the identified variations in the disease's severity in general and also in the populations' levels. Several factors can contribute to variation in disease presentation, including population density, gender and age differences, and comorbid circumstances including diabetes mellitus, hypertension, and obesity. Genetic factors presumably influence SARS-CoV-2 infection susceptibility. Besides this, COVID-19 has also been linked with a higher risk of mortality in men and certain ethnic groups, revealing that host genetic characteristics may affect the individual risk of death. Also, genetic variants involved in pathologic processes, including virus entrance into cells, antiviral immunity, and inflammatory response, are not entirely understood. Regarding SARS-CoV-2 infection characteristics, the present review suggests that various genetic polymorphisms influence virus pathogenicity and host immunity, which might have significant implications for understanding and interpreting the matter of genetics in SARS-CoV-2 pathogenicity and customized integrative medical care based on population investigation.

Cytotoxicity of metformin against HT29 colon cancer cells contributes to mitochondrial Sirt3 upregulation.

Cancer and diabetes, the two mitochondria-related diseases, have recently been linked to silent mating-type information regulation 2 homolog 3 (SIRT3) activity irregularities. In this study, the effect of metformin, an antidiabetic with anticancer properties, has been evaluated on mitochondrial functionality markers, cell death pathways, and SIRT3 enzyme activity in the colon cancer cell line, HT-29, and human embryonic kidney cells (HEK 293). HT-29 cells were treated with metformin (5, 10, 20, 40, and 80 µM) for 24, 48, and 72 h for measuring the IC50 concentration. Reactive oxygen species (ROS) production, apoptosis, mitochondrial membrane potential, SIRT3 activity, and expression were evaluated against the colon cancer cell line, HT-29. Results indicated a higher ROS production at 6 than 12 h with metformin treatment. Metformin modified the mitochondrial membrane potential, resulting in cell death induction. Results from SIRT3 activity and expression showed that metformin increased its activity and expression in cancer cells. In conclusion, metformin in HT-29 cells disturbed the mitochondrial activity via increased ROS levels and SIRT3 activity, and these rapid modifications may play a key role in its cytotoxic property.

Tropisetron attenuates tumor growth and progression in an experimental model of mouse lung cancer.

The antineoplastic effects of 5-hydroxytryptamine (5-HT) receptor antagonists have been shown in previous studies. However, the exact underlying mechanisms mediating these antineoplastic effects are unclear. In the present study, we assessed the antineoplastic effects of tropisetron, a 5-HT receptor antagonist, in an experimental model of lung cancer in BALB/c mouse. Lewis lung carcinoma cell line was used to induce lung cancer. Mice were divided into four groups (n = 6) as follows: tumor-bearing mice + tropisetron (5 mg/kg intraperitoneally [IP]), tumor-bearing mice + tropisetron (10 mg/kg IP), tumor-bearing mice + saline, healthy mice + tropisetron (10 mg/kg). Tumor burden, interferon-γ (IFN-γ), interleukin (IL)-4, pathological response, Ki-67, and E-cadherin were assessed using enzyme-linked immunosorbent assay, and real-time polymerase chain reaction. Comet assay was used to assess DNA toxicity. Tropisetrone-treated animals (either 5 or 10 mg/kg) showed significantly lower tumor sizes at the day 24th after tumor induction. Tropisetron received animals also showed significantly higher levels of IFN-γ, E-cadherin, pathologic response, and necrotic cells compared to the saline-treated counterparts. In addition, the levels of IL-4, and Ki-67 were significantly lower in tropisetrone treated mice in comparison with control. Furthermore, tropisteron coadministration signifcantly reduced H2 O2 -induced DNA toxicity while treatment with tropisteron alone showed no adverse effect on DNA. Tropisetrone can be used as a potential antineoplastic drug in lung cancer. This agent can promote its antineoplastic effects in part through modulating inflammatory and proliferating markers.

Association of Hemoglobin A1c and Wound Healing in Diabetic Foot Ulcers.

OBJECTIVE: This study evaluated the association between hemoglobin A1c (A1C) and wound outcomes in patients with diabetic foot ulcers (DFUs). RESEARCH DESIGN AND METHODS: We conducted a retrospective analysis of an ongoing prospective, clinic-based study of patients with DFUs treated at an academic institution during a 4.7-year period. Data from 270 participants and 584 wounds were included in the analysis. Cox proportional hazards regression was used to assess the incidence of wound healing at any follow-up time in relation to categories of baseline A1C and the incidence of long-term (≥90 days) wound healing in relation to tertiles of nadir A1C change and mean A1C change from baseline, adjusted for potential confounders. RESULTS: Baseline A1C was not associated with wound healing in univariate or fully adjusted models. Compared with a nadir A1C change from baseline of -0.29 to 0.0 (tertile 2), a nadir A1C change of 0.09 to 2.4 (tertile 3) was positively associated with long-term wound healing in the subset of participants with baseline A1C <7.5% (hazard ratio [HR] 2.07; 95% CI 1.08-4.00), but no association with wound healing was seen with the mean A1C change from baseline in this group. Neither nadir A1C change nor mean A1C change were associated with long-term wound healing in participants with baseline A1C ≥7.5%. CONCLUSIONS: There does not appear to be a clinically meaningful association between baseline or prospective A1C and wound healing in patients with DFUs. The paradoxical finding of accelerated wound healing and increase in A1C in participants with better baseline glycemic control requires confirmation in further studies.

Knockout of Angiotensin AT2 receptors accelerates healing but impairs quality.

Wounds are among the most common, painful, debilitating and costly conditions in older adults. Disruption of the angiotensin type 1 receptors (AT1R), has been associated with impaired wound healing, suggesting a critical role for AT1R in this repair process. Biological functions of angiotensin type 2 receptors (AT2R) are less studied. We investigated effects of genetically disrupting AT2R on rate and quality of wound healing. Our results suggest that AT2R effects on rate of wound closure depends on the phase of wound healing. We observed delayed healing during early phase of wound healing (inflammation). An accelerated healing rate was seen during later stages (proliferation and remodeling). By day 12, fifty percent of AT2R(-/-) mice had complete wound closure as compared to none in either C57/BL6 or AT1R(-/-) mice. There was a significant increase in AT1R, TGFß1 and TGFß2 expression during the proliferative and remodeling phases in AT2R(-/-) mice. Despite the accelerated closure rate, AT2R(-/-) mice had more fragile healed skin. Our results suggest that in the absence of AT2R, wound healing rate is accelerated, but yielded worse skin quality. Elucidating the contribution of both of the angiotensin receptors may help fine tune future intervention aimed at wound repair in older individuals.

Wind sock deformity in rectal atresia.

Rectal atresia is a rare anorectal deformity. It usually presents with neonatal obstruction and it is often a complete membrane or severe stenosis. Windsock deformity has not been reported in rectal atresia especially, having been missed for 2 years. A 2-year-old girl reported only a severe constipation despite having a 1.5-cm anal canal in rectal examination with scanty discharge. She underwent loop colostomy and loopogram, which showed a wind sock deformity of rectum with mega colon. The patient underwent abdominoperineal pull-through with good result and follow-up. This is the first case of the wind sock deformity in rectal atresia being reported after 2 years of age.