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BackgroundSince the introduction of laparoscopic surgery, it has become more popular with many advantages over open surgery including faster recovery, shorter hospital stays, and decreased tissue trauma. Despite its benefits, laparoscopic surgery can result in its own unique complications, such as the formation of a trocar site hernia (TSH), which have been reported in approximately 0–1.0% of laparoscopic cases when using non-bladed trocars.MethodsA literature review was performed from June 1990 to June 2019. PubMed was searched using the keywords “laparoscopic surgery,” “trocar site hernia,” and “port site hernia.” Only articles in English were identified but not limited to the USA.ResultsThe total number of patients in all articles was 18,533 with a mean follow-up period of 22.50 ± 1.76 months. The overall trocar site hernia rate was 0.104%. When comparing open vs. closed ports, there was no significant difference in the hernia incidence rate for 5-mm and 10-mm ports. When comparing bladed versus non-bladed trocars left open, there was a statistically significant difference with lower hernia incidence rates for non-bladed trocars over bladed trocars for 5-mm, 10-mm, and 12-mm ports. And when comparing trocar location from midline versus off-midline, there was a statistically significant higher TSH incidence in midline trocar locations.ConclusionResults suggest that TSH rate is lower when using non-bladed trocars for any size of trocar. When comparing whether fascial closure had an effect, the 5-mm and 10-mm ports had no difference in incidence rates and leaving the fascia open can reduce operative time, risk of needlestick injuries, and overall procedural cost. In addition, trocars at midline locations resulted in higher TSH incidence rates. Future research is still needed to assess for other factors that may influence hernia formation and how it can be minimized.

Background Obesity is a common disorder with a negative impact on IVF treatment outcome. It is not clear whether morbidly obese women (BMI >= 35 kg/m2) respond to treatment differently as compared to obese women (BMI = 30–34.9 kg/m2) in IVF. Our aim was to compare the outcome of IVF or ICSI treatments in obese patients to that in morbidly obese patients. Methods This retrospective cohort study was conducted in a tertiary care centre. Patients inclusion criteria were as follows; BMI ≥ 30, age 20–40 years old, first cycle IVF/ICSI treatment with primary infertility and long follicular pituitary down regulation protocol. Results A total of 406 obese patients (group A) and 141 morbidly obese patients (group B) satisfied the inclusion criteria. Average BMI was 32.1 ± 1.38 kg/m2 for group A versus 37.7 ± 2.99 kg/m 2 for group B. Patient age, cause of infertility, duration of stimulation, fertilization rate, and number of transferred embryos were similar in both groups. Compared to group A, group B had fewer medium size and mature follicles (14 vs. 16), fewer oocytes collected (7 vs. 9) and required higher doses of HMG (46.2 vs. 38.5 amps). There was also a higher cancellation rate in group B (28.3% vs. 19%) and lower clinical pregnancy rate per started cycle (19.9% vs. 28.6%). Conclusion In a homogenous infertile and obese patient population stratified according to their BMI, morbid obesity is associated with unfavorable IVF/ICSI cycle outcome as evidenced by lower pregnancy rates. It is recommended that morbidly obese patients undergo appropriate counseling before the initiation of this expensive and invasive therapy.

Acute heart failure (AHF) is one of the most common diseases in old age that can lead to mortality. Systemic hypoperfusion is associated with hepatic ischemia–reperfusion injury, which may be irreversible. Ischemic hepatitis due to AHF has been linked to the pathogenesis of liver damage. In the present study, we extensively investigated the role of mitochondrial dynamics-related proteins and their epigenetic regulation in ischemic liver injury following AHF and explored the possible hepatoprotective role of carvedilol. The biochemical analysis revealed that the ischemic liver injury following AHF significantly elevated the activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) enzymes, the level of total and direct bilirubin, and the expression of hepatic mitogen-activated protein kinase (MAPK), dynamin-1-like protein (DNM1L), and hepatic miRNA-17. At the same time, it significantly reduced the serum albumin level, the activity of hepatic superoxide dismutase (SOD), and the expression of mitochondrial peroxisome proliferator-activated receptor-1α (PGC-1α), and mitofusin 2 (Mtf2). The histological examination of the liver tissue revealed degenerated hepatocytes. Interestingly, administration of carvedilol either prior to or after isoprenaline-induced AHF significantly improved the liver function and reversed the deterioration effect of AHF-induced ischemic hepatitis, as demonstrated by biochemical, immunohistochemical, and histological analysis. Our results indicated that the hepatoprotective effect of carvedilol in ameliorating hepatic ischemic damage could be attributed to its ability to target the mitochondrial dynamics-related proteins (Mtf2, DNM1L and PGC-1α), but also their epigenetic regulator miRNA-17. To further explore the mode of action of carvedilol, we have investigated, in silico, the ability of carvedilol to target dynamin-1-like protein and mitochondrial dynamics protein (MID51). Our results revealed that carvedilol has a high binding affinity (−14.83 kcal/mol) toward the binding pocket of DNM1L protein. In conclusion, our study highlights the hepatoprotective pharmacological application of carvedilol to attenuate ischemic hepatitis associated with AHF.

Testicular torsion (TT) is the most common urological emergency in children and young adults that can lead to infertility in many cases. The ischemia-reperfusion (IR) injury due to TT has been implicated in the pathogenesis of testicular damage. The main pathological mechanisms of contralateral injury after ipsilateral TT are not fully understood. In the presented study, we investigated the molecular and microscopic basis of ipsilateral and contralateral testicular injury following ipsilateral testicular torsion detorsion (T/D) and explored the possible protective role of vitamin D3. The biochemical analysis indicated that IR injury following T/D significantly decreased the activity of testicular glutathione peroxidase (GPx) enzyme, level of serum testosterone, serum inhibin B, and expression of testicular miRNA145, while increased the activity of testicular myeloperoxidase (MPO) enzyme, level of testicular malondialdehyde (MDA), level of serum antisperm-antibody (AsAb), and expression of ADAM-17. The histological and semen analysis revealed that torsion of the testis caused damages on different tissues in testis. Interestingly, administration of vitamin D3 prior to the IR injury reversed the deterioration effect of IR injury on the testicular tissues as indicated by biochemical and histological analysis which revealed normal appearance of the seminiferous tubules with an apparent decrease in collagen fiber deposition in both ipsilateral and contralateral testes. Our results revealed that the protective effect of vitamin D3 treatment could be attributed to target miRNA145 and ADAM17 protein. To further investigate these findings, we performed a detailed molecular modelling study in order to explore the binding affinity of vitamin D3 toward ADAM17 protein. Our results revealed that vitamin D3 has the ability to bind to the active site of ADAM17 protein via a set of hydrophobic and hydrophilic interactions with high docking score. In conclusion, this study highlights the protective pharmacological application of vitamin D3 to ameliorate the damages of testicular T/D on the testicular tissues via targeting miRNA145 and ADAM17 protein.

Alcoholism is one of the most common diseases that can lead to the development of several chronic diseases including steatosis, and cognitive dysfunction. Statins are lipid-lowering drugs that are commonly prescribed for patients with fatty liver diseases; however, the exact effect of statins on cognitive function is still not fully understood. In the present study, we have investigated the molecular and microscopic basis of cognitive impairment induced by alcohol and/or Atorvastatin (ATOR) administration to male Wistar albino rats and explored the possible protective effect of acetylsalicylic acid (ASA). The biochemical analysis indicated that either alcohol or ATOR or together in combination produced a significant increase in the nucleotide-binding domain–like receptor 3 (NLRP3), interleukin-1β (IL-1β) miRNA155 expression levels in the frontal cortex of the brain tissue. The histological and morphometric analysis showed signs of degeneration in the neurons and the glial cells with aggregations of inflammatory cells and a decrease in the mean thickness of the frontal cortex. Immunohistochemical analysis showed a significant increase in the caspase-8 immunoreaction in the neurons and glial cells of the frontal cortex. Interestingly, administration of ASA reversed the deleterious effect of the alcohol and ATOR intake and improved the cognitive function as indicated by biochemical and histological analysis. ASA significantly decreased the expression levels of miRNA155, NLRP3, and IL1B, and produced a significant decrease in caspase-8 immunoreaction in the neurons and glial cells of the frontal cortex with a reduction in the process of neuroinflammation and neuronal damage. To further investigate these findings, we have performed an extensive molecular docking study to investigate the binding affinity of ASA to the binding pockets of the NLRP3 protein. Our results indicated that ASA has high binding scores toward the active sites of the NLRP3 NACHT domain with the ability to bind to the NLRP3 pockets by a set of hydrophilic and hydrophobic interactions. Taken together, the present study highlights the protective pharmacological effect of ASA to attenuate the deleterious effect of alcohol intake and long term ATOR therapy on the cognitive function via targeting miRNA155 and NLRP3 proteins.

Autism spectrum disorders (ASD) represent a diverse group of neuropsychiatric conditions, and recent evidence has suggested a connection between ASD and microbial dysbiosis. Immune and gastrointestinal dysfunction are associated with dysbiosis, and there are indications that modulating the microbiota could improve ASD-related behaviors. Additionally, recent findings highlighted the significant impact of microbiota on the development of autoimmune liver diseases, and the occurrence of autoimmune liver disease in children with ASD is noteworthy. In the present study, we conducted both an in vivo study and a clinical study to explore the relationship between indomethacin-induced dysbiosis, autoimmune hepatitis (AIH), and the development of ASD. Our results revealed that indomethacin administration induced intestinal dysbiosis and bacterial translocation, confirmed by microbiological analysis showing positive bacterial translocation in blood cultures. Furthermore, indomethacin administration led to disturbed intestinal permeability, evidenced by the activation of the NLRP3 inflammasomes pathway and elevation of downstream biomarkers (TLR4, IL18, caspase 1). The histological analysis supported these findings, showing widened intestinal tight junctions, decreased mucosal thickness, inflammatory cell infiltrates, and collagen deposition. Additionally, the disturbance of intestinal permeability was associated with immune activation in liver tissue and the development of AIH, as indicated by altered liver function, elevated ASMA and ANA in serum, and histological markers of autoimmune hepatitis. These results indicate that NSAID-induced intestinal dysbiosis and AIH are robust triggers for ASD existence. These findings were further confirmed by conducting a clinical study that involved children with ASD, autoimmune hepatitis (AIH), and a history of NSAID intake. Children exposed to NSAIDs in early life and complicated by dysbiosis and AIH exhibited elevated serum levels of NLRP3, IL18, liver enzymes, ASMA, ANA, JAK1, and IL6. Further, the correlation analysis demonstrated a positive relationship between the measured parameters and the severity of ASD. Our findings suggest a potential link between NSAIDs, dysbiosis-induced AIH, and the development of ASD. The identified markers hold promise as indicators for early diagnosis and prognosis of ASD. This research highlights the importance of maintaining healthy gut microbiota and supports the necessity for further investigation into the role of dysbiosis and AIH in the etiology of ASD.

The impact of Moringa oleifera leaf ethanol extract (MOLEE) was assessed on the expression of the steroidogenic genes (steroidogenic acute regulatory protein ( StAR ) and cytochrome P450c17 subfamily a ( CYP17a ) and luteinizing hormone receptor ( LHR ) gene) as well as on the cadmium chloride (CdCl 2 )–induced reproductive toxicity for 56 days in male rats. Four groups were used: control, Moringa-treated (MOLEE), CdCl 2 -treated, and CdCl 2 + MOLEE groups. The reproductive toxicity of CdCl 2 was confirmed; it caused a significant decrease in the accessory sex organ weights, testosterone level, testicular GST level, elevated MDA level (lipid peroxidation indicator), and histopathological alterations in seminiferous tubules, prostate, seminal vesicles, and epididymis as well as sperm characteristics. It also induced downregulation in the expression of StAR and CYP17a genes without change in the expression LHR gene. Eleven active compounds were detected in the GC-MS analysis of MOLEE; six of them have antioxidant properties, and five new compounds presented variable activities. MOLEE alone induced a stimulatory effect on the expression of steroidogenic and LHR genes. It restored the weight of reproductive organs to the control level; however, the recovery in sperm count, motility, abnormalities, percentage of alive sperm, testosterone, and MDA level are still comparable with the control level. Similar findings were also reported at the histological structure of the testes, epididymis, and accessory sex glands. Complete recovery of the GST enzyme activity was observed. Additionally, a restoration in the expression level of the steroidogenic genes was also reported. Our results indicated that the concurrent administration of MOLEE with CdCl 2 can partially mitigate its harmful effects on male fertility.

Objectives: During the COVID-19 pandemic, a quick and reliable phone-triage system is critical for early care and efficient distribution of hospital resources. The study aimed to assess the accuracy of the traditional phone-triage system and phone triage-driven deep learning model in the prediction of positive COVID-19 patients. Setting: This is a retrospective study conducted at the family medicine department, Cairo University. Methods: The study included a dataset of 943 suspected COVID-19 patients from the phone triage during the first wave of the pandemic. The accuracy of the phone triaging system was assessed. PCR-dependent and phone triage-driven deep learning model for automated classifications of natural human responses was conducted. Results: Based on the RT-PCR results, we found that myalgia, fever, and contact with a case with respiratory symptoms had the highest sensitivity among the symptoms/ risk factors that were asked during the phone calls (86.3%, 77.5%, and 75.1%, respectively). While immunodeficiency, smoking, and loss of smell or taste had the highest specificity (96.9%, 83.6%, and 74.0%, respectively). The positive predictive value (PPV) of phone triage was 48.4%. The classification accuracy achieved by the deep learning model was 66%, while the PPV was 70.5%. Conclusion: Phone triage and deep learning models are feasible and convenient tools for screening COVID-19 patients. Using the deep learning models for symptoms screening will help to provide the proper medical care as early as possible for those at a higher risk of developing severe illness paving the way for a more efficient allocation of the scanty health resources.

Hepatitis C virus (HCV) is a widely spread disease all over the world. HCV has very high mutation rate that makes it resistant to antibodies. Modeling HCV to identify the virus mutation process is essential to its detection and predicting its evolution. This paper presents a model of HCV based on profile hidden Markov model (PHMM) architecture. An iterative model learning procedure is proposed and applied to both full-length sequence of virus and its very high variation (mutation) zone called NS5A. A pilot study on HCV dataset of type 4 is conducted which is of special concern in Egypt.

Hepatitis C virus (HCV) is a widely spread disease all over the world. HCV has very high mutation rate that makes it resistant to antibodies. Modeling HCV to identify the virus mutation process is essential to its detection and predicting its evolution. This paper presents a model based framework for estimating mutation rate of HCV in two steps. Firstly profile hidden Markov model (PHMM) architecture was builder to select the sequences which represents sequence per year. Secondly mutation rate was calculated by using pair-wise distance method between sequences. A pilot study is conducted on NS5B zone of HCV dataset of genotype 4 subtype a (HCV4a) in Egypt.