Enhancement of porous asphalt mixtures modified with various fibers and ethylene-vinyl acetate polymer.

Porous asphalt mixture is conventional hot mix asphalt (HMA) with substantially decreased fines, which produces an open-graded mixture that enables the water to flow through an interconnected void space. Porous asphalt is a permeable system that has a lot of benefits. However, because of its open structure, the durability of this mixture decreases, and both its stability and resilient modulus are much lower compared to the dense conventional asphalt mixtures. Also, the high void percentage may lead to an increase in the draindown proportion. Fibers (cellulose or mineral) and polymer-modified binders are recommended for porous asphalt mixtures, especially in hot and moderate climates. The objective of this study is to improve the porous asphalt mixture's performance by using ethylene-vinyl acetate (EVA) polymer-modified bitumen. Two types of fibers (cellulose fibers and glass wool fibers) were used, separately to determine the control mixture. Four different proportions of EVA polymer were added to the bitumen (1%, 2%, 3%, and 4%) and Scanning Electron Microscopy (SEM) was used for better investigating of the bitumen microstructure, then The Marshall mix design was used to determine the optimum EVA content (OEC) for the porous asphalt mixture. Several performance tests were conducted to investigate the characteristics of the porous asphalt mixture, such as the infiltration rate, binder draindown, the wheel track and the cantabro abrasion tests. The findings of the study conclude that the addition of EVA polymer to the porous asphalt mixtures enhances the performance as it increases stability by 20.8% and the infiltration rate by 20.6%. It decreases binder draindown proportion by 33.3%, cantabro abrasion loss by 25.1% and the rut depth at 5,000 cycles and 10,000 cycles by 29.8% and 19.7%, respectively.

Interrogating the estrogen-mediated regulation of adrenocortical Klotho expression using ovariectomized albino rat model exposed to repeated restraint stress.

Reproductive aging is associated with altered stress response and many other menopausal symptoms. Little is known about the adrenal expression of the anti-aging protein Klotho or how it is modulated by estrogen in ovariectomized stressed rats. Fifty-six Wistar female rats were assigned into seven equal groups. Sham-operated (Sham), sham stressed (Sham/STS), ovariectomized (OVR), ovariectomized stressed (OVR/STS), ovariectomized stressed rosiglitazone-treated (OVR/STS/R), ovariectomized stressed estrogen-treated (OVR/STS/E), and ovariectomized stressed estrogen/GW9662 co-treated (OVR/STS/E/GW) groups. All stressed rats were subjected daily to a one-hour restraint stress test for 19 days. At the end of the experiment, blood was collected for serum corticosterone (CORT) analysis. Adrenal tissues were obtained and prepared for polymerase chain reaction (PCR) assay, hematoxylin and eosin (H&E), immunohistochemistry-based identification of Klotho and PPAR-γ, and Oil Red O (ORO) staining. The rise in serum CORT was negligible in the OVR/STS group, in contrast to the Sham/STS group. The limited CORT response in the former group was restored by estrogen and rosiglitazone and blocked by estrogen/GW9226 co-administration. ORO-staining revealed a more evident reduction in the adrenal fat in the OVR/STS group, which was reversed by estrogen and counteracted by GW. Also, there was a comparable expression pattern of Klotho and PPAR-γ in the adrenals. The adrenal Klotho decreased in the OVR/STS group, but was reversed by estrogen treatment. GW9226/estrogen co-treatment interfered with the regulatory effect of estrogen on Klotho. The study suggested modulation of the adrenal Kotho expression by estrogen, in the ovariectomized rats subjected to a restraint stress test. This estrogen-provided adrenal protection might be mediated by PPAR-γ activation.

Targeting NF-κB/COX-2 signaling by soyasaponin I alleviates diclofenac-induced gastric ulceration in male albino rats.

Gastric ulceration is a prevalent worldwide clinical presentation due to altered gastric defense mechanisms. Nonsteroidal anti-inflammatory drugs are one of the common causes of gastric ulcers mediated by the release of inflammatory mediators. The study aimed to investigate the potential protective effect of soyasaponin I (soya) against diclofenac (DIC)-induced gastric ulcer in rats and to highlight the underlying mechanisms. The experiment was conducted on 40 male Wistar albino rats, equally distributed into five groups: control, DIC-induced ulcer (9 mg/kg/d, orally, twice daily for 3 days), ulcer/soya-, ulcer/ranitidine-, and ulcer/soya/selective nuclear factor kappa B inhibitor (JSH-23)-treated groups. The doses of soya, ranitidine, and JSH were 20, 25, and 5 mg/kg/d, respectively, given orally. Gastric specimens were prepared for gene and histological study and for biochemical analysis of gastric prostaglandin E2 (PGE2), oxidative markers, and inflammatory cytokines. The gastric samples were formalin-fixed, paraffin-embedded, and subjected to hematoxylin and eosin (H&E), PAS staining, and immunohistochemical assay for identification of nuclear factor kappa B (NF-κB), cyclooxygenase-2 (COX-2), and proliferation marker (Ki67) expressions. The findings revealed decreased gastric PGE2 and altered inflammatory and oxidative markers in the ulcer model group. The H&E staining showed mucosal injury characterized by mucosal surface defects and inflammatory cell infiltrations. The polymerase chain reaction (PCR) and immunohistochemistry demonstrated an upregulation of NF-κB and COX-2 expression at gene/protein levels; meanwhile, Ki67 downregulation. The soya-treated group showed maintained biochemical, histological, and PCR findings comparable to the ranitidine-treated group. The JSH-23-treated group still showed partial gastric protection with biochemical and immunohistochemical changes. Soyasaponin I ameliorated DIC-induced gastric ulcers by targeting the COX-2 activity through modulation of NF-κB signaling.

"Challenges and concerns faced by parents of a group of Egyptian children with cleft lip/palate: a qualitative study".

BACKGROUND: Cleft lip and palate are the most common developmental anomalies that affect the mouth and related structures. They can both affect children physiologically, socially, and functionally and lead to psychological distress in their parents. The present study aims to understand the challenges parents of cleft lip and palate patients face in Egypt, elucidate how they cope with these challenges, and assess their concerns for the future. METHODS: For the present phenomenological qualitative exploration, the parents of cleft lip and palate patients attending the cleft care clinic were invited to participate in the study through face-to-face recruitment at the clinic. An interview guide about the research question was developed to include standardized open-ended questions providing a framework for structured discussions. The interviews were audio-recorded after obtaining written informed consent from participants then collected data were transcribed for data analysis. RESULTS: Of the 12 participants, there were nine mothers and three fathers. Their children's ages ranged from 1.5 years to 19 years and had different presentations of cleft lip and palate from unilateral cleft lip to complete bilateral cleft lip and palate. Feeding difficulty was one of the main challenges encountered by the parents. At the same time, fear of being subjected to bullying was the main concern for the future of their children. Six themes were noted that were continually reported: Health & Wellbeing; Parental emotions; Parental attitudes & behaviors; Financial aspects; Relationship aspects; and Career/Education. CONCLUSIONS: There were 4 factors that directly impacted the themes, namely: the type of cleft, gender of the child, gender role of the parent, and the age of the child impacted the parental concerns and the challenges faced under the influence of sociocultural beliefs and existing support systems.

ACE2/ACE imbalance mediates bisphenol A-induced lung injury in Wistar rats: Results from captopril versus losartan histo-biochemical study.

Bisphenol-A (BPA) is a synthetic chemical compound broadly used in the plastic and epoxy resin industries with a considerable potential for food contamination. Literary reports have suggested that the altered renin-angiotensin system (RAS) is a mechanism for lung injury and inflammation caused by variable agents. The current study sought to investigate the contribution of RAS to BPA-induced lung damage. Moreover, the study assessed whether angiotensin II and/or bradykinin pathways were involved. For this aim, the angiotensin-converting enzyme (ACE) inhibitor captopril (Cap), either alone or combined with bradykinin receptor antagonist icatibant (Icat), was attempted versus the angiotensin receptor blocker losartan (Los). An eight-week study was conducted on forty Wistar male albino rats randomly divided into five equal groups: control, BPA, BPA/Cap, BPA/Los, and BPA/Cap/Icat groups. Captopril (100 mg/mL) and losartan (200 mg/mL) were given orally in drinking water, but icatibant (Icat) was injected subcutaneously (250 µg/kg) during the last two weeks of captopril treatment. Biochemical analysis of bronchoalveolar lavage fluid (BALF) and lung tissues, polymerase chain reaction (PCR) assay for ACE, ACE2, and caspase-3 genes expression, and histological and immunohistochemical studies were carried out to evaluate BPA-mediated pulmonary inflammation/apoptosis. BPA impaired the histological structure of the lungs, increased ACE, ACE2, and caspase-3 expressions at both gene/protein levels, and increased BALF inflammatory cytokines and lung oxidative markers. Inhibiting the ACE activity by captopril maintained the histological lung injury score, restored inflammation and the ACE2/ACE balance, and decreased apoptosis. Further improvement was obtained by the angiotensin II receptor (ATR1) blocker losartan. Icatibant (bradykinin B2 receptor blocker) didn't counteract the observed captopril effects. It was strongly suggested that RAS contributed to BPA-induced lung damage via alteration of ACE2 and ACE expression mediating angiotensin II generation rather than bradykinin.

Bisphenol-A exposure alters liver, kidney, and pancreatic Klotho expression by HSP60-activated mTOR/autophagy pathway in male albino rats.

The effect of bisphenol-A (BPA) on Klotho protein (aging-suppressing protein) expression in different body organs has not been sufficiently addressed by literature studies. The study investigated the impact of BPA on Klotho expression in multiple organs including the liver, kidney, and pancreas and suggested the involved molecular pathways. Twenty-seven male Wistar albino rats were divided into 3 equal groups: control, low-dose BPA (4.5 µg/L), and high-dose BPA (8 µg/L) groups in drinking water for 45 consecutive days. Liver, kidney, and pancreatic specimens were prepared for a gene study of Klotho, HSP60, mTOR, and ULK1 mRNA expressions. Also, the tissue specimens were measured for malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) levels. Paraffin-embedded sections were also prepared and subjected to Hematoxylin and Eosin (H&E) staining and immunohistochemical detection of Klotho and HSP60. The results revealed an alteration in the MDA, SOD, NO tissue levels, disturbed gene expression profile, and apoptotic changes in the histological findings of the examined organs which were obvious (p < 0.05) in the high-dose group. The anti-aging Klotho gene/protein expression was reduced (p < 0.05) more in the high-dose BPA group than in the low dose. In contrast, HSP60 gene/protein expression was significantly increased (p < 0.05) more in the high dose. It was concluded that BPA exposure contributed to cell stress and markedly reduced Klotho protein expression in liver, kidney, and pancreatic tissues, possibly by modulation of the HSP60-activated mTOR/autophagy signaling.

Modeling the Effects of Cypermethrin Toxicity on Ovalbumin-Induced Allergic Pneumonitis Rats: Macrophage Phenotype Differentiation and p38/STAT6 Signaling Are Candidate Targets of Pirfenidone Treatment.

Although the classic form of asthma is characterized by chronic pneumonitis with eosinophil infiltration and steroid responsivity, asthma has multifactorial pathogenesis and various clinical phenotypes. Previous studies strongly suggested that chemical exposure could influence the severity and course of asthma and reduce its steroid responsiveness. Cypermethrin (CYP), a common pesticide used in agriculture, was investigated for the possible aggravation of the ovalbumin (OVA)-induced allergic pneumonitis and the possible induction of steroid resistance in rats. Additionally, it was investigated whether pirfenidone (PFD) could substitute dexamethasone, as an alternative treatment option, for the induced steroid resistance. Fifty-six male Wistar albino rats were randomly divided into seven groups: control, PFD alone, allergic pneumonitis, CYP alone, allergic pneumonitis/CYP-exposed, allergic pneumonitis/CYP/dexamethasone (Dex), and allergic pneumonitis/CYP/PFD-treated groups. Allergic pneumonitis was induced by three intraperitoneal OVA injections administered once a week, followed by an intranasal OVA instillation challenge. CYP (25 mg/kg/d), Dex (1 mg/kg/d), and PFD (100 mg/kg/d) were administered orally from day 15 to the end of the experiment. Bronchoalveolar lavage fluid (BALF) was analyzed for cytokine levels. Hematoxylin and eosin (H&E) and periodic acid Schiff (PAS)-stained lung sections were prepared. Immunohistochemical identification of p38 MAPK and lung macrophages was performed. The inflammatory/oxidative status of the lung and PCR-quantification of the STAT6, p38 MAPK, MUC5AC, and IL-13 genes were carried out. The allergic pneumonitis-only group showed eosinophil-mediated inflammation (p < 0.05). Further CYP exposure aggravated lung inflammation and showed steroid-resistant changes, p38 activation, neutrophil-mediated, M1 macrophage-related inflammation (p < 0.05). All changes were reversed (p < 0.05) by PFD, meanwhile not by dexamethasone treatment. Pirfenidone could replace dexamethasone treatment in the current rat model of CYP-induced severe steroid-resistant asthma via inhibiting the M1 macrophage differentiation through modulation of the STAT6/p38 MAPK pathway.

Stroke intervention and pharmacotherapy guidelines: Knowledge-to-practice translation gaps among the emergency resident physicians in Riyadh, Saudi Arabia.

Translating the updated medical guidelines into routine clinical practice is an important initiative to improve the population's health and decrease disease outcomes. A cross-sectional survey-based study was conducted in Riyadh City, Saudi Arabia, to evaluate the knowledge and degree of application (practice) of the stroke management guidelines among emergency resident physicians. An interview-based self-administered questionnaire was used to survey the emergency resident doctors in Riyadh hospitals from May 2019 to January 2020. Of 129 participants, 78 valid, complete responses were obtained (60.5% response rate). Descriptive statistics, principle component, and correlation analyses were used. Most resident doctors were men(69.4%) with a mean age of 28.4±3.37 years. More than 60% of the residents were satisfied with their knowledge of the stroke guidelines; meanwhile, 46.2% were satisfied with their application of the guidelines. Both Knowledge and practice compliance components were significantly and positively correlated. Also, both components were significantly correlated with being updated, aware of, and strictly following these guidelines. The mini-test challenge showed a negative result with a mean knowledge score of 1.03±0.88. Even though the majority of participants utilized different tools of education and were aware of the American Stroke Association Guidelines. It was concluded that a considerable gap in the residents' knowledge regarding the current stroke management guidelines was present in Saudi hospitals. Also, it was reflected on their actual implementation and application into clinical practice. Continuous medical education, training, and follow-up of the emergency resident doctors, administered as a part of the government health programs, are crucial to improve the health care delivery for acute stroke patients.

Modulatory effects of concomitant quercetin/sitagliptin administration on the ovarian histological and biochemical alterations provoked by doxorubicin in a streptozotocin-induced diabetic rat model.

Limited literature was available on the effects of sitagliptin or quercetin treatments on doxorubicin induced ovarian dysfunction in diabetic animals. The study aim was test the efficacy and suggested mechanisms of quercetin/sitagliptin combined treatment on the doxorubicin-induced ovarian toxicity in rat model with streptozotocin-induced diabetes. Forty eight female Wistar rats were divided into six groups: 1) Control; 2) Streptozotocin induced diabetes; 3) Streptozotocin-induced diabetes + doxorubicin ovarian damage; 4) Streptozotocin-induced diabetes + doxorubicin ovarian damage with; 5) Streptozotocin-induced diabetes + doxorubicin ovarian damage with sitagliptin treatment and 6) Streptozotocin-induced diabetes + doxorubicin ovarian damage with concomitant quercetin/sitagliptin treatment. Biochemical tests for serum estrogen, progesterone, insulin, blood glucose, and ovarian levels of malondialdehyde, nitric oxide, and superoxide dismutase and qRT-PCR for NOBOX, FSHr, and iNOS genes were performed. Histological evaluation was done on ovary sections with hematoxylin and eosin and immunohistochemistry for 8-OHdG and iNOS followed by morphometric analysis. The streptozotocin-induced diabetic group showed varying degrees of follicle atresia and altered biochemical parameters, both were marked in the streptozotocin-induced diabetic + doxorubicin group. The mRNA of NOBOX, FSHr, and iNOS genes were disturbed with increased immunoexpression of iNOS and 8-OHdG. Quercetin and/or sitagliptin administration improved all altered histological and biochemical parameters and was more effective as a combined treatment. The study suggested equal efficacy of both quercetin and sitagliptin in mitigating the doxorubicin-induced ovarian toxicity in the streptozotocin diabetic rat model, and the combined therapy showed anti-inflammatory, anti-antioxidant, and anti-DNA damage mechanisms.

Synthetic Graft Augmentation Is Safe and Effective for the Repair of Acute Achilles Tendon Rupture in Patients With Preexisting Tendinopathy.

Purpose: To assess the safety and report the clinical outcomes of synthetic graft augmentation using polypropylene (PP) mesh in the repair of acute Achilles tendon (AT) rupture in patients with preexisting tendinopathy. Methods: Patients who underwent open repair for acute AT rupture at our institution between April 2017 and March 2019 were retrospectively identified. The inclusion criteria were acute AT rupture in patients with preexisting tendinopathy. All patients included in the study underwent acute repair augmented by an inlay PP mesh and had 30 months' follow-up. Patient characteristics, operative details, and outcomes were analyzed. Continuous data were described by mean, standard deviation, median, and range. The Wilcoxon signed rank test was used to analyze the change in patient-reported outcome measures. The significance level was set at a P-value of .05. Results: Thirteen patients were included. There were 5 female and 8 male patients, withan average age of 52 years (range 49-56 years). No cases of rerupture or graft-related complications requiring additional treatment occurred during mean follow -up of 38 months. All patients reported good functional outcome, as shown from nonsignificant difference between the preinjury and 38-month postoperative Achilles Tendon Rupture Score (88.5 ± 2.2 vs 89.2 ± 2.2, P = .107) and the excellent postoperative American Orthopedic Foot and Ankle Society Ankle/Hindfoot Scale score (92.22 ± 2.2) at last follow-up. At the end of follow-up, all patients were able to perform single-legged heel rise as the noninvolved side. By average of 16 weeks, all patients returned to their preinjury activity level. Conclusions: The use of inlay PP mesh to augment the repair of acute AT rupture in patients with preexisting tendinopathy appears to be safe and effective, allowing early return to preinjury activity level with favorable clinical outcomes. Level of Evidence: Level IV, therapeutic case series.

Apoptotic susceptibility of pancreatic alpha cells to environmentally relevant dose levels of bisphenol-A versus dibutyl phthalate is mediated by HSP60/caspase-3 expression in male albino rats.

Unfortunately, humanity is exposed to mixed plasticizers such as bisphenol-A (BPA) and dibutyl phthalate (DBP) that are leached from the daily used plastic products. Previous studies have demonstrated their potential in pancreatic beta cell injury and diabetes induction. The study hypothesized that both compounds would affect the pancreatic alpha cells in albino rats when administered at environmentally relevant doses. Heat shock protein 60 (HSP60) and caspase-3 protein expression was also investigated as potential mechanisms. Thirty-six male Wistar albino rats were separated into four equal groups: control, BPA alone, DBP alone, and BPA + DBP combined groups. BPA and DBP were given in drinking water for 45 days in a dose of 4.5 and 0.8 µg/L, respectively. Fasting blood glucose, serum insulin, pancreatic tissue levels of malondialdehyde, and superoxide dismutase were measured. Pancreatic sections were subjected to hematoxylin & eosin (H & E) staining, glucagon, HSP60, and caspase-3 immunohistochemistry. Although all three experimental groups showed diffuse islet cell HSP60 immunoreactivity, rats exposed to BPA alone showed α-cell-only apoptosis, indicated by H & E changes and caspase-3 immunoreactivity, associated with reduced glucagon immunoreaction. However, rats exposed to DBP alone showed no changes in either α or ß-cells. Both combined-exposed animals displayed α and ß apoptotic changes associated with islet atrophy and reduced glucagon expression. In conclusion, the study suggested HSP60/caspase-3 interaction, caspase-3 activation, and initiation of apoptosis in α-cell only for BPA-alone exposure group, meanwhile DBP alone did not progress to apoptosis. Interestingly, both α/ß cell effect was observed in the mixed group implying synergetic/additive action of both chemicals when combined.

Histomorphological Changes in a Rat Model of Polycystic Ovary Syndrome and the Contribution of Stevia Leaf Extract in Modulating the Ovarian Fibrosis, VEGF, and TGF-ß Immunoexpressions: Comparison with Metformin.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder of fertile females. It has been reported that stevia leaf extract (SLE) has antidiabetic and antihyperlipidemic properties. Therefore, the current study hypothesized and investigated the role and mechanistic aspects of a natural sweetener; SLE in treating a rat model of letrozole-induced PCOS and to compare it with metformin. Thirty-five female Wistar albino rats were divided into 5 groups: control, PCOS-induced group (letrozole, 1 mg/kg/d, for 21 days), SLE, metformin, and combination-treated groups (300 mg/kg/d, for the next 28 days in SLE and metformin-treated groups). Vaginal smears were done. The levels of glucose, lipid, and hormonal profiles were measured in the serum meanwhile, malonyl dialdehyde (MDA), superoxide dismutase (SOD), and tumour necrosis factor (TNF-α) were measured in the ovary. Ovarian sections were subjected to hematoxylin and eosin, Masson, and immunohistochemical identification of VEGF and TGF-ß followed by morphometric analysis. PCOS rats showed altered hormonal and lipid profiles, in addition to hyperglycemia. Also, the ovarian tissue levels of MDA and TNF-α were elevated, and SOD was decreased. Numerous cystic follicles, decrease/absence of corpora lutea, interstitial fibrosis with positive VEGF and TGF-ß immunoreactivity were evident. SLE improved all altered parameters. SLE showed potential therapeutic merits in letrozole-induced PCOS via anti-inflammatory, antioxidant, anti-fibrotic, and angiogenesis regulating mechanisms. Its effects were almost comparable to metformin, and the combination of both has no further synergistic effect.

The anti-tumour effect of induced pluripotent stem cells against submandibular gland carcinoma in rats is achieved via modulation of the apoptotic response and the expression of Sirt-1, TGF-ß, and MALAT-1 in cancer cells.

The era of induced pluripotent stem cells (iPSCs) was used as novel biotechnology to replace embryonic stem cells bypassing the ethical concerns and problems of stem cell transplant rejection. The anti-tumour potential of iPSCs against many tumours including salivary cancer was proven in previous studies. The current study aimed to investigate the contribution of the Bax, Sirt-1, TGF-ß, and MALAT genes and/or their protein expression to the pathogenesis of submandibular carcinogenesis before and after iPSCs treatment. Thirty Wistar albino rats were equally assigned into three groups: group I (control), group II (Squamous cell carcinoma (SCC)): submandibular glands were injected SCC cells, and group III (SCC/iPSCs): SCC rats were treated by 5 × 106 iPSCs. Submandibular gland sections were subjected to histological and immunohistochemical analyses to detect mucopolysaccharides, Bax, and TGF-ß expression as well as PCR quantification for TGF-ß, Sirt-1, and lncRNA MALAT-1 gene expressions. Western blotting was also used to detect Sirt-1 and TGF-ß protein expressions. SCC group revealed infiltration by sheets of malignant squamous cells with or without keratin pearls and inflammatory cells, in addition to upregulation of TGF-ß, Sirt-1, MALAT-1, and Bax, whereas SCC/iPSCs group showed an improved submandibular histoarchitecture with the maintenance of the secretory function. Bax and TGF-ß immunoexpression were significantly reduced. The upregulated TGF-ß, Sirt-1, and MALAT-1 genes were significantly decreased. iPSCs protected against the experimentally induced submandibular gland carcinoma that might be achieved via their regenerative potential and their regulatory modulation of Sirt-1, TGF-ß, and MALAT-1 gene/protein expressions and of the apoptotic response in cancer cells.

The biomechanistic aspects of renal cortical injury induced by diesel exhaust particles in rats and the renoprotective contribution of quercetin pretreatment: Histological and biochemical study.

Although several studies have reported a toxic effect of diesel exhaust particles (DEP) exposure on the kidney tissues, the involvement of autophagy/NF-kB signaling as encountered mechanisms and the protective effects of a natural flavonoid, quercetin on DEP remains unclear. Thirty-two albino rats were divided as control, quercetin-treated (60 mg/kg, oral), DEP-exposed (0.5 mg/kg, intra-tracheal), and quercetin/DEP-exposed groups. Specimens of the renal cortex were subjected to histo-biochemical study and immunohistochemical analysis using anti-NF-kB, and anti-LC3ß antibodies followed by morphometric and statistical analyses. The expression level of autophagy genes was quantitatively evaluated using RT-PCR, as well. The DEP-exposed rats showed an elevation in the renal tissue levels of MDA and a decrease in the catalase and superoxide dismutase (p < .05). Histologically, there were cytoplasmic vacuolar changes in the lining cells of the renal tubules, glomerular atrophy, and vascular congestion. In addition, renal inflammation was evident as confirmed by the increased NF-kB immunoexpression. Moreover, the gene expression of Becn1, ATG5, and LC3ß increased (p <. 0) due to DEP exposure. Conversely, quercetin pretreatment improved these renal histo-biochemical alterations (p < .05) and regulated autophagy/NF-kB pathways. Overall, the study proved the renal toxicity mediated by DEP exposure via precipitating renal inflammation, autophagy activation, and oxidative stress. Quercetin pretreatment could antagonize such machinery to protect the kidney against DEP.

Technical Innovations to Reduce Complication Rates in Esophageal Atresia with Particular Reference to Long-term Outcomes: A Single Surgeon's Experience of 22 Years.

Background: Following esophageal atresia/tracheoesophageal fistula (EA/TEF) repair, the standard leak rate reported in the literature is 5%-10%, and stricture rate is 40%-72%. There is a global quest for surgical innovations to drive down these complication rates which can cause considerable morbidity. Methods: A prospectively maintained database of the senior author's patients who had esophageal atresia repair from 1995 to 2016 was reviewed. Two distinct innovations were implemented: (1) adequate or generous mobilization of the lower esophageal pouch and (2) a 2-5 mm slit in distal esophagus to widen its circumference. Results: Forty-three patients with EA/TEF were reviewed. Of those, 40 underwent primary repair. The median follow-up was 12.5 years (range 4-26 years). There were no anastomotic leaks and only 8 (20%) patients developed anastomotic strictures requiring dilations (1-5 dilations/patients). One patient (2.5%) had a recurrent fistula. One early mortality was recorded. At the latest follow-up, 35 (87.5%) patients had normal oral feeding, while 1 (2.5%) patient had occasional food sticking episodes. Four syndromic patients (10%) were on jejunal or gastrostomy feeding. Conclusion: An adequate or generous mobilization of the distal esophageal pouch, together with a 2-5 mm slit in the distal esophagus, achieves a tension-free and wide anastomosis. All anastomoses eventually narrow, sometimes just a little, and starting on a higher scale with a small slit, helps. These seemingly minor innovations, when used together, contributed to a substantially lower complication rate sustained over a 22-year period - no leaks and only 20% stricture rate.

A real-life correlation between clinical SYNTAX score II and carotid intima-media thickness in patients with stable coronary artery disease.

BACKGROUND: SYNTAX score II (SSII) is an update of the established SYNTAX score (SS) that uses clinical variables such as age, sex, creatinine clearance, left ventricular ejection fraction, chronic obstructive pulmonary disease, and peripheral arterial disease. Furthermore, SSII has been proven to be a more powerful predictive tool than SS in patients with complex coronary artery disease (CAD). Carotid õntima-media thickness (CIMT) is a widely used noninvasive evidence for subclinical or early atherosclerosis, and it was proved to be an independent predictor for cardiovascular events. Most of the previously published articles studied the association between the CIMT with old cardiovascular scoring systems such as SSI and Gensini score with debatable data about their correlation. AIM: To study the correlation between SSII and CIMT in stable CAD patients undergoing elective coronary angiography (CA). METHOD AND PATIENTS: A prospective study including 155 patients undergoing elective CA for stable CAD excluding patients with history of acute coronary syndrome, previous coronary revascularization either by percutaneous coronary intervention or coronary artery bypass grafting, and previous cerebrovascular stroke. RESULTS: The mean age of patients was 58.25 ± 16.46 years, and 79 patients (50.96%) were men. The mean SSII score was 10.23 ± 11.36 and mean CIMT was 0.85 ± 0.24. The correlation between SSII and CIMT using Spearman correlation showed a strong correlation between SSII score and CIMT with correlation coefficient r = 0.752. CONCLUSION: The study showed a strong positive correlation between SSII and CIMT in stable CAD patients undergoing elective CA.

The short-term impact of COVID-19 pandemic on spine surgeons: a cross-sectional global study.

PURPOSE: The outbreak of COVID-19 erupted in December 2019 in Wuhan, China. In a few weeks, it progressed rapidly into a global pandemic which resulted in an overwhelming burden on health care systems, medical resources and staff. Spine surgeons as health care providers are no exception. In this study, we try to highlight the impact of the crisis on spine surgeons in terms of knowledge, attitude, practice and socioeconomic burden. METHODS: This was global, multicentric cross-sectional study on 781 spine surgeons that utilized an Internet-based validated questionnaire to evaluate knowledge about COVID-19, availability of personal protective equipment, future perceptions, effect of this crisis on practice and psychological distress. Univariate and multivariate ordinal logistic regression analyses were used to evaluate the predictors for the degree of COVID-19 effect on practice. RESULTS: Overall, 20.2%, 52% and 27.8% of the participants were affected minimally, intermediately and hugely by COVID-19, respectively. Older ages (ß = 0.33, 95% CI 0.11-0.56), orthopedic spine surgeons (ß = 0.30, 95% CI 0.01-0.61) and those who work in the private sector (ß = 0.05, 95% CI 0.19-0.61) were the most affected by COVID-19. Those who work in university hospitals (ß = - 0.36, 95% CI 0.00 to - 0.71) were affected the least. The availability of N95 masks (47%) and disposable eye protectors or face shields (39.4%) was significantly associated with lower psychological stress (p = 0.01). Only 6.9%, 3.7% and 5% had mild, moderate and severe mental distress, respectively. CONCLUSION: While it is important to recognize the short-term impact of COVID-19 pandemic on the practice of spine surgery, predicting where we will be standing in 6-12 months remains difficult and unknown. The COVID-19 crisis will probably have an unexpected long-term impact on lives and economies.

"In situ similis" Culturing of Plant Microbiota: A Novel Simulated Environmental Method Based on Plant Leaf Blades as Nutritional Pads.

High-throughput cultivation methods have recently been developed to accelerate the recovery of microorganisms reluctant to cultivation. They simulate in situ environmental conditions for the isolation of environmental microbiota through the exchange of growth substrates during cultivation. Here, we introduce leaf-based culture media adopting the concept of the plant being the master architect of the composition of its microbial community. Pre-physical treatments of sunflower plant leaves, namely punching, freezing, and/or autoclavation, allowed the diffusion of electrolytes and other nutrients to configure the leaf surface as a natural pad, i.e., creating an "in situ similis" environment suitable for the growth of rarely isolated microbiota. We used surface inoculation and membrane-filtration methods to assess the culturability of endophytic bacteria from the sunflower phyllosphere and rhizosphere. Both methods supported excellent colony-forming unit (CFU) development when compared to standard R2A medium, with a special affinity to support better growth of epiphytic and endophytic populations of the phyllosphere compared with the rhizosphere. A 16S rRNA gene analysis of >122 representative isolates indicated the cultivation of a diverse set of microorganisms by application of the new methods. It indicated the predominance of 13 genera of >30 potential species, belonging to Firmicutes, Proteobacteria, and Actinobacteria, and especially genera not commonly reported for sunflower, e.g., Rhizobium, Aureimonas, Sphingomonas, Paracoccus, Stenotrophomonas, Pantoea, Kosakonia, and Erwinia. The strategy successfully extended diversity and richness in the endophyllosphere compared to the endorhizosphere, while CFUs grown on the standard R2A medium mainly pertain to Firmicutes, especially Bacillus spp. MALDI-TOF MS analysis clustered the isolates according to their niche and potential functions, where the majority of isolates of the endorhizosphere were clustered away from those of the endophyllosphere. Isolates identified as Gammaproteobacteria and Alphaproteobacteria were distinguishably sub-clustered, which was in contrast to the heterogeneous isolates of Firmicutes (Bacillus spp.). In conclusion, leaf in situ similis cultivation is an effective strategy to support the future application of culturomics of plant microbiota. This is an effort to access novel isolates that are more adapted and competitive in their natural environments, especially those subjected to abiotic stresses like those prevailing in arid/semi-arid zones, and, consequently, to support the application of agro-biotechnologies, among other technologies, to improving agriculture in such zones.

Insufflation in minimally invasive surgery: Is there any advantage in staying low?

AIM: Minimally invasive repair of esophageal atresia with tracheoesophageal fistula (EA/TEF) and congenital diaphragmatic hernia (CDH) is feasible and confers benefits compared to thoracotomy or laparotomy. However, carbon dioxide (CO2) insufflation can lead to hypercapnia and acidosis. We sought to determine the effect of lower insufflation pressures on patients' surrogate markers for CO2 absorption - arterial partial pressure of CO2 (PaCO2), end tidal CO2 (EtCO2) and pH. METHODS: Single center retrospective review, including neonates without major cardiac anomaly. Selected patients formed 2 groups: Historical pressure (HP) group and low pressure (LP) group. We reported on the patients' preoperative characteristics that potentially confound the degree of CO2 absorption or elimination. Outcome measures were perioperative PaCO2, EtCO2, arterial pH and anesthetic time. RESULTS: 30 patients underwent minimally invasive surgery for CDH and 24 patients for EA/TEF with similar distribution within the HP and LP group. For CDH patients as well as for EA/TEF patients, there were no significant differences in their preoperative characteristics or surgery duration comparing HP and LP groups. With a decrease in insufflation pressure in CDH patients, there were a significant decrease (p = 0.002) in peak PaCO2 and an improvement in nadir pH (p = 0.01). For the EA/TEF patients, the decrease in insufflation pressure was associated with a significant decrease (p = 0.03) in peak EtCO2. Considering all 54 patients, we found EtCO2 to be highly significantly inversely correlated with pH and positively correlated with intraoperative PaCO2 (p < 0.001). Baseline Hb was inversely correlated with mean EtCO2 (p < 0.001). CONCLUSION: With lower insufflation pressures, CDH patients had significantly improved hypercapnia and acidosis, while EA/TEF patients had significantly reduced EtCO2. EtCO2 was correlated with acidosis and hypercapnia. TYPE OF STUDY: Retrospective case control study. LEVEL OF EVIDENCE: Level III.