C3-Spirooxindoles: Divergent chemical synthesis and bioactivities (2018-2023).

This scientific review documents the recent progress of C3-spirooxindoles chemistry (synthesis and reaction mechanism) and their bioactivities, focusing on the promising results as well as highlighting the biological mechanism via the reported molecular docking findings of the most bioactive derivatives. C3-Spirooxindoles are attractive bioactive agents and have been found in a variety of natural compounds, including alkaloids. They are widely investigated in the field of medicinal chemistry and play a key role in medication development, such as antivirals, anticancer agents, antimicrobials, etc. Regarding organic synthesis, several traditional and advanced strategies have been reported, particularly those that started with isatin derivatives.

A meta analysis on the utility of Anakinra in severe COVID-19 disease.

BACKGROUND AND OBJECTIVE: The most important presentation of COVID-19 is hyper inflammatory condition and cytokine storm that occurs due to excessive increase of the inflammatory mediators specially, pro-inflammatory interleukins such as IL-1ß, IL-6 and tumor necrosis factor-α which have an important role in the cytokine storm pathway. Up till now there is not a definitive treatment for COVID-19 disease, but according to the pathophysiology of the disease, Anakinra (Interleukin- 1 inhibitor) is an adjuvant treatment option in patients with severe COVID-19 by blocking the effect of IL-1. So, we aimed to summarize the studies that evaluated the safety and efficacy of Anakinra in patients diagnosed with COVID-19. METHODS: We performed a search in PubMed, Cochrane Library, Scopus, and Web of Science (WOS) databases from inception till 7 Jan 2022. Additionally, we searched randomized and non-randomized clinical trials, cohort, case series, case control, case report more than 3 patients which contain confirmed cases of COVID-19 who received Anakinra (Interleukin- 1 inhibitor) for the management of hyper-inflammatory condition associated with COVID-19 disease. A meta-analysis was conducted using review manager 5.4. RESULTS: We included 44 articles in the systematic review. Ultimately, 23 studies were incorporated in the meta-analysis with a total number of 3179 patients. Our analysis showed statistically significant difference in the following outcomes: duration of ICU stays [MD = -0.65, 95% CI (-1.09, -0.03), p = 0.04], the number of patients who needed invasive mechanical ventilation [RR = 0.57, 95% CI (0.39, 0.84), p = 0.004], and number of deaths [RR = 0.80, 95% CI (0.66, 0.99), p = 0.04]. Our analysis showed no statistically significant difference in the following outcomes: length of hospital stays [MD = -0.16, 95% CI (-0.42, 0.11), p = 0.26], oxygen-free days [MD = -0.81, 95% CI (-3.81, 2.20), p = 0.60], and the number of patients who needed non-invasive mechanical ventilation [RR = 1.09, 95% CI (0.47, 2.52), p = 0.84]. CONCLUSION: Anakinra showed some promising results in important outcomes related to COVID-19 as it significantly reduced the rate of mortality and the need of invasive mechanical ventilation. It should be used in severe cases more than mild and moderate cases to avoid possible immunosuppression complications. Anakinra use is safe in cases of COVID-19 at dose less than 100 mg. Another important outcome was significant reduction is the D-dimer level. Anakinra may be effective in the treatment of specific immunocompromised cases, but it should be used cautiously.

Hepatic ß-arrestins: potential roles in liver health and disease.

Β-arrestins are intracellular scaffolding proteins that have multifaceted roles in different types of disorders. In this review article, we gave a summary about the discovery, characterization and classification of these proteins and their intracellular functions. Moreover, this review article focused on the hepatic expression of ß-arrestins and their hepatocellular distribution and function in each liver cell type. Also, we showed that ß-arrestins are key regulators of distinct types of hepatic disorders. On the other hand, we addressed some important points that have never been studied before regarding the role of ß-arrestins in certain types of hepatic disorders which needs more research efforts to cover.

Targeting necroptosis in fibrosis.

Necroptosis, a type of programmed cell death that resembles necrosis, is now known to depend on a different molecular mechanism from apoptosis, according to several recent studies. Many efforts have reported the possible influence of necroptosis in human disorders and concluded the crucial role in the pathophysiology of various diseases, including liver diseases, renal injuries, cancers, and others. Fibrosis is the most common end-stage pathological cascade of several chronic inflammatory disorders. In this review, we explain the impact of necroptosis and fibrosis, for which necroptosis has been demonstrated to be a contributing factor. We also go over the inhibitors of necroptosis and how they have been applied to fibrosis models. This review helps to clarify the role of necroptosis in fibrosis and will encourage clinical efforts to target this pathway of programmed cell death.

The molecular mechanisms underlying anti-inflammatory effects of galangin in different diseases.

When used as an alternative source of drugs to treat inflammation-associated diseases, phytochemicals with anti-inflammatory properties provide beneficial impacts. Galangin is one of the most naturally occurring flavonoids. Galangin has many biological activities, such as anti-inflammatory, antioxidant, antiproliferative, antimicrobial, anti-obesity, antidiabetic, and anti-genotoxic activities. We observed that galangin was well tolerated and positively impacted disease underlying inflammation for the renal, hepatic, central nervous system, cardiovascular, gastrointestinal system, skin, and respiratory disorders, as well as ulcerative colitis, acute pancreatitis, retinopathy, osteoarthritis, osteoporosis, and rheumatoid arthritis. Galangin anti-inflammatory effects are mediated mainly by suppressing p38 mitogen-activated protein kinases, nuclear factor-kappa B, and nod-like receptor protein 3 signals. These effects are confirmed and supported by molecular docking. Clinical translational research is required to accelerate the bench-to-bedside transfer and determine whether galangin can be utilised as a safe, natural source of pharmaceutical anti-inflammatory medication for humans.

"Anosmia" the mysterious collateral damage of COVID-19.

COVID-19 pandemic spreads worldwide, with more than 100 million positive cases and more than 2 million deaths. From the beginning of the COVID-19 pandemic, several otolaryngologists described many cases of a sudden loss of smell (anosmia) associated with the disease with or without additional symptoms. Anosmia is often the first and sometimes the only sign in the asymptomatic carriers of COVID-19. Still, this disorder is underestimated, and it is not life-threatening. However, it significantly decreases the quality of life. This olfactory dysfunction continues in several cases even after the nasopharyngeal swab was negative. The occurrence of anosmia can be used as a screening tool for COVID-19 patients and can be used to identify these patients to accomplish the isolation and tracking procedures. In this review, we highlighted the possible mechanisms of anosmia in COVID-19 patients, major pathologies and features of anosmia, implications of anosmia in early diagnosis of COVID-19, evaluation of the smell function during COVID-19, and management and treatment options of COVID-19 anosmia.

Acute and chronic metabolic effects of carvedilol in high-fructose, high-fat diet-fed mice: implication of ß-arrestin2 pathway.

We aimed to investigate the acute and chronic effects of carvedilol on insulin resistance in high-fructose, high-fat diet (HFrHFD) - fed mice and the implication of the ß-arrestin2 pathway. The acute effect of carvedilol (10 mg/kg, i.p.) on glucose tolerance and hepatic lipid signaling in normal and insulin resistant mice was investigated. Then, the chronic effect of carvedilol on insulin resistance and dyslipidemia in HFrHFD-fed mice was examined. Changes in ß-arrestin2 and its downstream signals in liver, skeletal muscle, and adipose tissue were measured. This involved measuring phosphatidylinositol 4,5-bisphosphate (PIP2) and diacylglycerol (DAG) levels and protein kinase B (AKT) activity. Carvedilol acutely reduced fasting blood glucose levels in both normal and insulin resistant mice without significantly affecting the glucose tolerance. These acute effects were associated with increased hepatic PIP2 but decreased hepatic DAG levels. Chronic administration of carvedilol significantly ameliorated insulin resistance and dyslipidemia in HFrHFD-fed mice. These chronic effects were associated with increased ß-arrestin2, PIP2, and AKT activity levels but decreased DAG levels in the classical insulin target tissues. In conclusion, carvedilol acutely maintains glucose homeostasis and chronically ameliorates insulin resistance and dyslipidemia in HFrHFD-fed mice. The insulin sensitizing effects of carvedilol are highly correlated with the upregulation of ß-arrestin2 pathway.

Hospitalization of unintentional fall injuries in Kuwait: a national database study.

BACKGROUND: Accidental falls are a major cause of morbidity placing pressure on hospital capacity and utilizing costly services. Evaluating the burden of falls is key for planning, implementation, and evaluation of prevention strategies. To date, no studies have been published on accidental falls at the population level in Kuwait. We studied the burden of accidental falls on public hospital inpatient capacity in Kuwait and identified the subgroups with the highest utilization of inpatient service days. METHODS: From the national database of inpatient hospitalizations, we selected hospitalizations of patients admitted to Kuwait's public hospitals for unintentional injury caused by an accidental fall from 1 January through 31 December 2016. We studied the number of inpatient service days (bed days), length of stay (LOS), and number of hospitalizations by age group, gender, and nationality. Mann-Whitney, Kruskal-Wallis, and Chi square tests were used for comparison. Logistic regression was used to quantify the risk of prolonged LOS and fractures among fall-related hospitalizations. RESULTS: Accidental falls were responsible for 2.9% of inpatient hospitalizations, 3.7% of inpatient service days (61,140 days) with an ALOS of 9.1 days in Kuwait's public hospitals in 2016. Accidental falls were responsible for 4.6% of older adult service days, and an even higher 5.6% of older women service days. In the age group 13-64, fall-related service days for non-Kuwaitis (5.7%) were more than triple those for Kuwaitis (1.8%) with a substantial percentage among male non-Kuwaitis (8.1%). The risk factors for exceeding the national ALOS for fall-related hospitalizations were female gender (OR 1.36), age 65 and older (OR 9.72), age 13-64 (OR 5.20), being non-Kuwaiti (OR 1.39), sustaining a femur fracture (OR 11.67), and undergoing surgery (OR 2.63). Fall-related hospitalizations associated with a higher risk of fractures were females (OR 1.22), patients 65 years and older (OR 5.09), patients aged 13-64 (OR 3.65), and non-Kuwaitis (OR 1.28). CONCLUSIONS: Accidental falls impose a considerable burden on inpatient service utilization in Kuwait. This varies by age, gender, and nationality. To reduce this burden, prevention programs should target working-age non-Kuwaiti males and older females.

Pioglitazone Enhances ß-Arrestin2 Signaling and Ameliorates Insulin Resistance in Classical Insulin Target Tissues.

INTRODUCTION: Pioglitazone is a thiazolidinedione oral antidiabetic agent. This study aimed to investigate the effects of pioglitazone as insulin sensitizer on ß-arrestin2 signaling in classical insulin target tissues. METHODS: Experiments involved three groups of mice; the first one involved mice fed standard chow diet for 16 weeks; the second one involved mice fed high-fructose, high-fat diet (HFrHFD) for 16 weeks; and the third one involved mice fed HFrHFD for 16 weeks and received pioglitazone (30 mg/kg/day, orally) in the last four weeks of feeding HFrHFD. RESULTS: The results showed significant improvement in the insulin sensitivity of pioglitazone-treated mice as manifested by significant reduction in the insulin resistance index. This improvement in insulin sensitivity was associated with significant increases in the ß-arrestin2 levels in the adipose tissue, liver, and skeletal muscle. Moreover, pioglitazone significantly increased ß-arrestin2 signaling in all the examined tissues as estimated from significant increases in phosphatidylinositol 4,5 bisphosphate and phosphorylation of Akt at serine 473 and significant decrease in diacylglycerol level. CONCLUSION: To the best of our knowledge, our work reports a new mechanism of action for pioglitazone through which it can enhance the insulin sensitivity. Pioglitazone increases ß-arrestin2 signaling in the adipose tissue, liver, and skeletal muscle of HFrHFD-fed mice.

Effect of imidazoline-1 receptor agonists on renal dysfunction in rats associated with chronic, sequential fructose and ethanol administration.

Insulin resistance and chronic alcoholism are risk factors for renal dysfunction. This study investigated the therapeutic effects of two imidazoline-1 receptor (I1R) agonists on renal dysfunction in rats after chronic, sequential fructose and ethanol administration. Daily drinking water was supplemented with fructose (10%, w/v) for 12 weeks and then with ethanol (20%, v/v) for another 8 weeks. Rats were treated with rilmenidine and clonidine in the last two weeks of the study. Blood glucose and serum insulin (sIns) levels, lipid profiles, kidney function and renal histopathology were evaluated at the end of the experiment. Additionally, renal gene expression of nischarin, phosphatidylcholine-specific phospholipase C (PC-PLC) and prostaglandin E2 (PGE2) were measured. Renal levels of superoxide dismutase (SOD), malondialdehyde (MDA), myeloperoxidase (MPO), inducible nitric oxide synthase (iNOS) and total NO (tNO) were detected, and we determined the relative renal gene expression levels of alpha smooth muscle actin (α-SMA), hydroxyproline, interleukin 10 (IL-10), tumour necrosis factor alpha (TNF-α) and caspase-3. The results showed significant deterioration of blood glucose, sIns, lipid profiles, kidney function and renal histopathology in fructose/ethanol-fed rats. Additionally, markers of inflammation, fibrosis, apoptosis and oxidative stress were upregulated. The administration of rilmenidine or clonidine significantly improved blood glucose and sIns levels and reduced renal dysfunction. Our work showed that chronic, sequential fructose and ethanol administration induced fasting hyperglycaemia and renal impairment, and these effects were ameliorated by I1R agonists.

Carvedilol protects against hepatic ischemia/reperfusion injury in high-fructose/high-fat diet-fed mice: Role of G protein-coupled receptor kinase 2 and 5.

Hepatic ischemia/reperfusion injury (H-IRI) is associated with irreversible liver damage. The current study aimed to investigate the protective effect of carvedilol against H-IRI in high-fructose high-fat diet (HFrHFD)-fed mice and the role of G protein-coupled receptor kinase 2 and 5 (GRK2 and GRK5). Mice were fed HFrHFD for 16 weeks; then mice were subjected to 30 min of ischemia followed by 1 h of reperfusion at the end of feeding period. Carvedilol (20 mg/kg, i.p.) was administered 30 min before ischemia. To explore the role of GRK2 and GRK5 in mediating carvedilol effects, paroxetine (GRK2 inhibitor, 10 mg/kg, i.p.) and amlexanox (GRK5 inhibitor, 25 mg/kg, i.p.) were administered 30 min before carvedilol administration. Liver function, histopathology and hepatic oxidative stress, as well as inflammatory and apoptotic markers were measured at the end of the experiment. In addition, adrenergic receptor downstream signals were measured in the liver. Results showed increased markers of liver injury (ALT and AST) in mice subjected to H-IRI. Moreover, liver injury was associated with slight collagen deposits as revealed by histopathology and elevated hepatic levels of oxidative stress, inflammatory and apoptotic markers. On the other hand, carvedilol protected mice against H-IRI and improved all associated pathological changes. Furthermore, pre-injection of either GRK2 or GRK5 inhibitor did not change carvedilol effects on serum ALT level and liver collagen deposits, while increased its antioxidant, anti-inflammatory and anti-apoptotic effects. In conclusion, carvedilol protects against H-IRI in HFrHFD-fed mice. GRK2 and GRK5 may not play a potential role in mediating this effect.

Early Autologous Blood-Patch Pleurodesis versus Conservative Management for Treatment of Secondary Spontaneous Pneumothorax.

BACKGROUND: Autologous blood-patch pleurodesis has been effectively utilized as a treatment option for the condition of secondary spontaneous pneumothorax (SSP). Moreover, it can be used with persistent air leak, with or without residual air space. However, there have been no robust reports for the optimal timing for autologous blood-patch pleurodesis. The aim of this study is to compare early autologous blood-patch pleurodesis with conservative management of SSP. METHODS: We conducted a randomized controlled study at the Menoufia University Hospital. A total of 47 patients with SSP were randomly allocated into two groups: group A (23 patients) received intrapleural instillation of 50 mL autologous blood 3 days after insertion of chest drain and group B (24 patients) managed conservatively. The duration required for air leak to seal, chest drainage duration, length of hospital stay, and the incidence of complications were compared and statistically analyzed. RESULTS: The duration of air leak, duration to drain removal, and length of hospital stay were all significantly shorter in group A than in group B. CONCLUSION: Early intrapleural instillation of autologous blood is successful in sealing air leak in patients with SSP with persistent air leak, who are not fit or not willing to undergo surgery. It is superior to conservative treatment or late instillation of autologous blood, even if their lungs are not fully expanded.

Sildenafil protects against bile duct ligation induced hepatic fibrosis in rats: Potential role for silent information regulator 1 (SIRT1).

Hepatic fibrosis is a potential health problem that may end with life-threatening cirrhosis and primary liver cancer. Recent studies point out to the protective effects of silent information regulator1 (SIRT1), against different models of organs fibrosis. This work aimed to investigate the possible protective effect of sildenafil (SIRT1 activator) against hepatic fibrosis induced by bile duct ligation (BDL). Firstly, three different doses of sildenafil (5, 10, 20mg/kg/day) were investigated; to detect the most protective one against BDL induced liver dysfunction and hepatic fibrosis. The most protective dose is then used; to study its effect on BDL induced SIRT1 downregulation, imbalance of oxidant/antioxidant status, increased inflammatory cytokines and fibrosis. Sildenafil (20mg/kg/day) was the most protective one, it caused upregulation of SIRT1, reduction of hepatic malondialdehyde (MDA) content, increase in expression of nuclear factor erythroid 2-related factor 2 (Nrf2), hemeoxygenease (HO)-1, reduced glutathione (GSH) content and superoxide dismutase (SOD) activity. Hepatic content of tumor necrosis factor-α (TNF-α) and nuclear factor κB (NFκB) expression & content displayed significant reductions with sildenafil treatment, Furthermore, sildenafil caused marked reductions of transforming growth factor (TGF)-ß content, expression of plasminogen activator inhibitor-1 (PAI-1), matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1), α-smooth muscle actin (α-SMA), fibronectin, collagen I (α1) and hydroxyproline content. However, sildenafil protective effects were significantly reduced by co-administration of EX527 (SIRT1 inhibitor). Our work showed, for the first time that, sildenafil has promising protective effects against BDL induced liver dysfunction and hepatic fibrosis. These effects may be, in part, mediated by up regulation of SIRT1.

GSK-3ß heterozygous knockout is cardioprotective in a knockin mouse model of familial dilated cardiomyopathy.

Glycogen synthase kinase-3ß (GSK-3ß) plays a central role in both cardiac physiology and pathology. Herein we want to clarify the role of GSK-3ß in familial dilated cardiomyopathy. We generated a mouse model carrying a heterozygous knockout mutation of GSK-3ß (GSK-3ß(+/-) KO), together with a ΔK210 knockin mutation in cardiac troponin T (ΔK210 cTnT KI), which was proved to be one of the genetic causes of familial dilated cardiomyopathy (DCM). GSK-3ß(+/-) KO prevented the slow and rapid deterioration in left ventricular systolic function accompanying heart failure (HF) in DCM mice with heterozygous and homozygous ΔK210 cTnT KI mutations, respectively. GSK-3ß(+/-) KO also prevented cardiac enlargement, myocardial fibrosis, and cardiomyocyte apoptosis and markedly reduced the expression of cardiac ß-myosin heavy chain isoform, indicative of HF, in DCM mice with homozygous ΔK210 cTnT KI mutation. GSK-3ß(+/-) KO also extended the life span of these DCM mice. This study suggests that the inhibition of GSK-3ß is cardioprotective in familial DCM associated with ΔK210 cTnT mutation.

Reversal of Left Ventricular Functions in Chronic Mitral Regurgitation after Mitral Valve Replacement.

BACKGROUND: Mitral valve regurgitation leads to deterioration of left ventricular functions if not treated early. We aimed to study the effect of mitral valve replacement on normalization of ejection fraction, remodeling of left ventricular dimensions, and left atrial reduction in patients with chronic mitral regurgitation. METHODS: Between December 2012 and August 2014, 45 patients with chronic mitral regurgitation underwent isolated mitral valve replacement. None of the patients had any other severe valvular or concomitant disease or severe coronary heart  disease. The patients were evaluated by echocardiography (preoperative, 1-week, and 1-year postoperative). The results were statistically analyzed by paired t test. RESULTS: Forty-five patients who underwent mitral valve replacement in our hospital were included in  the study. The group comprised 20 men and 25 women; the mean age was 31.8 ± 6.76 years. The mean  left ventricular ejection fraction was 61.09 ± 7.6 and decreased significantly to 59.04 ± 6.65 and 59.67 ± 6.56, 1-week and 1-year postoperative follow up, respectively. The left atrium showed significant reduction in size (4 ± 0.54 cm) at 1-year postoperative follow up, from (4.51 ± 0.57 cm) one-week postoperative, and from (5.55 ± 0.88 cm) preoperatively. The mean left ventricular end systolic diameter significantly decreased from 4.06 ± 0.65 cm preoperatively to 3.4 ± 0.4 cm, 1-week postoperative (P = .01), and also decreased significantly to 3.45 ± 0.51 cm at 1-year follow up postoperatively, but was higher than that at 1-week follow up. Also, the mean left ventricular end diastolic diameter decreased  significantly during periods of follow up (P < .001). CONCLUSION: Reversal of left ventricular functions and reduction of left-sided chamber dimensions are possible if early mitral valve replacement is considered in chronic mitral regurgitation before worsening of the condition.

Weaponizing chitosan and its derivatives in the battle against lung cancer.

Lung cancer (LC) is a crisis of catastrophic proportions. It is a global problem and urgently requires a solution. The classic chemo drugs are lagging behind as they lack selectivity, where their side effects are spilled all over the body, and these adverse effects would be terribly tragic for LC patients. Therefore, they could make a bad situation worse, inflict damage on normal cells, and inflict pain on patients. Since our confidence in classic drugs is eroding, chitosan can offer a major leap forward in LC therapy. It can provide the backbone and the vehicle that enable chemo drugs to penetrate the hard shell of LC. It could be functionalized in a variety of ways to deliver a deadly payload of toxins to kill the bad guys. It is implemented in formulation of polymeric NPs, lipidic NPs, nanocomposites, multiwalled carbon nanotubes, and phototherapeutic agents. This review is a pretty clear proof of chitosan's utility as a weapon in battling LC. Chitosan-based formulations could work effectively to kill LC cells. If a researcher is looking for a vehicle for medication for LC therapy, chitosan can be an appropriate choice.

Challenges of Integrating ICD 11 into Automatic Alerting Systems.

Automatic alerting systems (AASs) can identify adverse health events but emergency communication relies on human operators and natural languages. For complete automation, we need to code the diversity of adverse events in a granularity that supports optimal dispatches. Hence, AAs shall integrate with the International Classification of Diseases (ICD). The ICD-11 coding system includes chapters for external causes of injury. However, ICD-11 supports coding injury incidents in electronic health records (EHRs) after they have occurred, while disregarding integrating real-time injury reporting within its framework. We explore the potential challenges associated with integrating ICD-11 into AAS by analyzing external causes of morbidity or mortality and the dimensions of external causes as potential areas of integration. We recognize the themes: (i) incident of injury, (ii) mode of transport, (iii) indoor location, (iv) outdoor location, and (v) type of building, and identify four challenges: (i) conceptual differences between the two systems, (ii) injury identification, (iii) presence of entities below the shoreline in ICD-11, and (iv) lack of specificity in certain ICD-11 codes related to AASs. For easy integration of ICD-11 into AASs, we recommend an AAS data dictionary and propose ICD-11 updates related to external causes of injury.

An optimized design for motivated broadband LPDA antenna.

This paper presents a super wideband and high-gain log periodic dipole array (LPDA) antenna. The overall structure of the antenna was constructed using microwave studio computer simulation technology. The optimal sizes of the planned antenna are 39 × 10× 0.254 mm3. The engineered antenna arrangement is implemented on an RT5880 substrate as a dielectric medium. The LPDA is arranged in four arms that are equally spaced on both lines. The main 50Ω feeder line is partially grounded at the back of the substrate. A combination of circular director units is being studied and tuned in a regular pattern at a predefined distance from the antenna. An improvement in gain of 3 dBi is the response of the director units. The Conformist LPDA is adjusted to achieve a wide range of millimeter wave bands ranging from 40 to over 70 GHz. The antenna resonates at 60 GHz, where the maximum realized gain of 14.97 dBi is attained. The antenna was tested for utilization in the V-band involving wireless personal area network (WPAN) applications recommended by IEEE 802.11ad and IEEE 802.15.3c. The outcomes of the constructed antenna elements' tests and simulations agree fairly well. The proposed layout works better than previous efforts in this field.

Primary CNS Burkitt Lymphoma Presenting as Sudden Bilateral Blindness in a Patient With Underlying Kabuki Syndrome: A Case Report.

Burkitt lymphoma is an aggressive B-cell non-Hodgkin lymphoma (NHL). Primary CNS lymphoma (PCNSL) is a rare disease, and the subtype of Burkitt lymphoma presenting as a sole CNS lesion is an even rarer diagnosis. Acute sudden blindness is a rare presenting symptom of PCNSL or NHL in general. We present an interesting case of a four-year-old boy with dysmorphic features whose visual examination showed a sudden bilateral loss of vision. There was bilateral eye proptosis and complete ptosis. Extraocular muscles were fixed straight. The pupils were fixed and mid dilated bilaterally and there was grade 3/4 papilledema in both eyes. Neuroimaging showed a mass in the base of the skull, extending to orbits and sinuses. A cervical biopsy of the enlarged lymph nodes was taken and a histopathological diagnosis of Burkitt lymphoma was made. Genetic analysis showed a GNB1 mutation, and the patient was diagnosed with Kabuki syndrome by a pediatrician, based on characteristic dysmorphic features. Treatment with steroids and chemotherapy was initiated.

Comorbidity of depression and type 2 diabetes in Egypt results from the International Prevalence and Treatment of Diabetes and Depression (INTERPRET-DD) study.

BACKGROUND: Diabetes mellitus and depression are serious common diseases, and the number of people with both conditions is rising steadily. Depression in people with diabetes mellitus results in poorer prognosis through different mechanisms. On the other hand, the presence of diabetes in individuals with depression increases functional impairment that is associated with depression. AIMS: The study aimed to assess the prevalence and factors associated with depression among adults with type 2 diabetes mellitus attending a diabetes clinic in Cairo, Egypt. METHODS: A cross-sectional study was conducted among adult patients with diabetes type 2 attending a diabetes clinic in the endocrinology department in Ain Shams University Teaching Hospital, Cairo, Egypt. Data were collected through face-to-face interviews by trained psychiatrists and from patients' records. RESULTS: The prevalence of depression among diabetic patients was 21.8% (95% CI [15.6%, 29.1%]). Depression was more common among younger age groups and those with a higher level of education. There was no significant difference between those with lifetime depression compared to those without depression regarding physical health complications. CONCLUSIONS: The prevalence of depression among patients with type 2 diabetes is high. Given the impact of co-morbid diabetes and depression, diabetic patients should be routinely screened for the latter condition.