Incidence and outcome of laryngeal edema and rhabdomyolysis after ingestion of black rock.

BACKGROUND: Black rock, Kala Pathar or ParaPhenyleneDiamine (PPD), is an aromatic amine widely used as a hair dye ingredient and is also used in textile industries. However, when ingested, PPD is highly toxic resulting in angioneurotic edema, rhabdomyolysis, acute kidney injury, toxic hepatitis, and myocarditis with a high mortality rate. This study aimed to evaluate the incidence and outcome of laryngeal edema and rhabdomyolysis after ingestion of PPD. PATIENTS AND METHODS: The current research was a cross-sectional study that was conducted at Aswan University Hospital, Aswan, Egypt, from December 2021 to December 2022. It consisted of 100 people who attempted suicide by ingesting black rock. All patients underwent general examinations and investigations, including complete blood count, urea, creatinine, creatine phospho kinase, alanine aminotransferase, aspartate aminotransferase, calcium, uric acid, phosphorus, urine analysis, and electrocardiography. RESULTS: The current study consisted of 15 males and 85 females; the most common presentation was stridor (88%) followed by muscle weakness (50%). Twelve percent of patients with stridor required tracheostomy while 14% required tracheal intubation. Regarding the complications of PPD ingestion, the incidence of hepatic injury was (97%) and acute kidney injury (14%) five of them required hemodialysis, with a mortality rate of 13%. Cardiac arrhythmias were noticed in the form of sinus tachycardia (24%), sinus bradycardia (3%), atrial fibrillation (5%), ventricular fibrillation (6%), and ventricular tachycardia (7%). Our study found a significant positive correlation between creatine phosphokinase, muscle weakness, and acute kidney injury (P = 0.005). Whereas a significant positive correlation was noted between stridor, hospital stay, and mortality rate (P = 0.000), (P = 0.003), respectively. Moreover, a significant positive correlation was found between tracheotomy, mortality rate, and hospital stay (P = 0.000). CONCLUSION: PDD toxicity is more frequent in younger females. The intoxication from the black rock is increasingly used in suicide attempts and vital organs are usually affected especially the kidney, liver, and heart causing morbidity and mortality.

Bee gomogenat enhances the healing process of diabetic wounds by orchestrating the connexin-pannexin gap junction proteins in streptozotocin-induced diabetic mice.

Delay in wound healing remains one of diabetes's worse side effects, which increases mortality. The proposed study sought to scrutinize the implications of bee gomogenat (BG) on diabetic's wound closure in a streptozotocin-(STZ)-enhanced type-1 diabetes model's rodents. We used 3 different mice groups: group 1 non-diabetic rodents "serving as control", group 2 diabetic rodents, and group3 BG-treated diabetic rodents. We noticed that diabetic rodents experience a delayed wound closure, which emerged as a significant (*P < 0.05) decline in the deposition of collagen as compared to control non-diabetic animals. We noticed that diabetic rodents have a delayed wound closure characterized by a significant (*P < 0.05) decrease in the CD31 expression (indicator for wound angiogenesis and neovascularization) and an apparent elevation in the expression of such markers of inflammation as MCP-1 and HSP-70 as compared to control animals. Moreover, diabetic animals displayed a significant (*P < 0.05) increase in the expression of gap junction proteins Cx43 and a significant decrease in the expression of Panx3 in the wounded skin tissues when compared to the controls. Intriguingly, topical application with BG on the diabetic wounded skin tissues contributes to a significant (#P < 0.05) enhancing in the collagen deposition, up-regulating the level of CD31 expression and a significant (#P < 0.05) down-regulation in the MCP-1 and HSP-70 expressions as compared to diabetic non-treated animals. The expression's levels of Cx43 and Panx3 were significantly (#P < 0.05) retrieved in diabetic rodents after BG treatment. Taken together, our findings showed for the first time that BG promotes the recovering process and accelerated the closure of diabetic related wounds.

Different Aspects of Diabetes in Hospitalized Patients with COVID-19.

Background: The novel severe acute respiratory syndrome coronavirus (SARS-CoV-2) causes COVID-19, a recent infectious disease that aggravates the underlying pathophysiology of hyperglycemia in diabetic individuals. This study aimed to detect how diabetes mellitus (DM) affected COVID-19 patients' morbidity and mortality, and the incidence of neonset DM. Patients and Methods: The present study was a cross-sectional study done at Aswan Isolation Hospitals, Egypt. It comprised 200 individuals who had been tested positive for COVID-19. They were divided into two groups: group 1 (pre-existing diabetes = 143 patients) and group 2 (new-onset diabetes = 57 patients), and all patients were subjected to general examinations, hospital stay duration, and investigations, such as (complete blood count, urea, creatinine, HBA1c, fasting, postprandial, and random blood sugar, D-Dimer, ferritin, C-reactive protein, PCR for SARS COV-2 RNA, and CT chest. Results: The current study consisted of 94 males and 106 females. According to disease severity, they were 96 (48.0%) critical cases, 57 (28.5%) severe cases, and 47 (23.5%) non-severe cases. The incidence of new-onset DM in COVID-19 patients was 28.5% (57 new cases), with a mortality rate of 42.0% (84 cases). Regarding glycemic control, we found a significant difference in fasting blood sugar (FBS) between the two groups, with a significant increase of FBS in the dead group than in the survived group. We also found a significant age difference in critical than in severe and non-severe groups, with a high mortality rate in older patients. Inflammatory markers, such as ferritin, CRP, and D-dimer, were higher in critical than in severe and non-severe groups. Conclusion: The prevalence of new-onset DM is significant among hospitalized COVID-19 patients. Older patients were more prone to disease severity with high mortality rate. Inflammatory markers such as CRP and ferritin were significantly related to the COVID-19 severity and outcome.

Molecular mechanisms underlying antitumor activity of camel whey protein against multiple myeloma cells.

Treating drug-resistant cancer cells is a clinical challenge and it is also vital to screen for new cancer drugs. Multiple myeloma (MM) is a plasma cell clonal cancer that, despite many experimental therapeutics, remains incurable. In this study, two MM cell line lines U266 and RPMI 8226 were used to determine the impact of camel whey protein (CWP). The CWP IC50 was calculated by MTT examination, while the flow cytometry analysis was used to investigate the chemotaxis responses of MM cells in relation to CXCL12 and the pro-apoptotic effect of CHP. MM cells were treated with CWP and Western blot analysis was used to determine the underlying molecular mechanisms. Dose and time based on the impact of CWP on the cell viability of MM cells with IC50 of 50 µg/ml, without affecting the viability of normal healthy PBMCs. CWP reduced chemotaxis of MM cells significantly from the CXC chemokine ligand 12 (CXCL12). Using Western blot analysis, we found that CWP decreased the activation of AKT, mTOR, PLCß3, NFαB and ERK, which was mechanistically mediated by CXCL12/CXCR4. In both U266 and RPMI 8226, CWP induced apoptosis by upregulating cytochrome C expression. In addition, CWP mediated the growth arrest of MM cells by robustly decreasing the expression of the anti-apoptotic Bcl-2 family members Bcl-2, Bcl-XL and Mcl-1. Conversely, the expression of pro-apoptotic Bcl-2 family members Bak, Bax and Bim was increased after treatment with CWP. Our data indicates CWP's therapeutic potential for MM cells.

Enhanced immune responses, PI3K/AKT and JAK/STAT signaling pathways following hepatitis C virus eradication by direct-acting antiviral therapy among Egyptian patients: a case control study.

The use of direct-acting antivirals (DAAs) therapy for the treatment of hepatitis C virus (HCV) results in a high-sustained virological response (SVR) and subsequently alters liver immunologic environment. However, hepatocellular carcinoma (HCC) may occur after DAAs treatment. We aimed to clarify changes of immune responses, PI3K/AKT and JAK/STAT signaling pathways in HCV-induced liver diseases and HCC following DAAs treatment. Four cohorts were classified as chronic HCV patients, HCV-related cirrhosis without HCC, HCV-related cirrhosis and HCC, and healthy control group. The patient groups were further divided into treated or untreated with DAAs with SVR12. Increased percentages of CD3, CD8 and CD4, decreased CD4/FoxP3/CD25, CD8/PD-1 and CD19/PDL-1 were found in DAAs-treated patients in the three HCV groups. Following DAAs therapy, the levels of ROS, IL-1ß, IL-6, IL-8 and TNF-α were significantly decreased in the three HCV groups. Treated HCV patients showed up regulation of p-AKT and p-STAT5 and down regulation of p-STAT3, HIF-1α and COX-2. In conclusion, DAAs enhance the immune response in chronic HCV and liver cirrhosis, hence our study is the first to show change in PI3K/AKT and JAK/STAT signaling pathways in different HCV-induced liver diseases after DAAs. In chronic HCV, DAAs have better impact on the immune response while in liver cirrhosis not all immune changes were prominent.

Cardiovascular System Affection and Its Relation to First-Year Mortality in Patients Initiating Maintenance Hemodialysis.

BACKGROUND: The incidence of end-stage renal disease (ESRD) has increased by 30-40% in the last decade. These patients have a higher mortality rate of 3-8 times compared to the general population. In the present study, we aimed to detect cardiovascular complications and their relation to the first-year mortality rate in patients on hemodialysis in Aswan University Hospital, upper Egypt. PATIENTS AND METHODS: Our study was a cross-sectional study which was done at the hemodialysis unit in Aswan University Hospital from May 2016 to May 2018. The study included 100 patients with ESRD on regular hemodialysis (first year on programmed hemodialysis). All patients were subjected to full clinical examination and laboratory studies includngd complete blood count (CBC), kidney function tests, serum calcium and phosphorus level, parathormone (PTH) hormone, serum albumin level, C-reactive protein (CRP), echocardiography and electrocardiogram (ECG), and lateral abdominal x-ray for detection of aortic calcification. . RESULTS: The present study included 47 males and 53 females, with a mean age of 50.6 ±13.89 years. The main risk factors for patients with ESRD were hypertension (48%) followed by diabetic nephropathy (36%), glomerulonephritis (15%), idiopathic etiology (11%), obstructive uropathy (8%), lupus nephritis (6%), polycystic kidney disease (4%) and cardio renal syndrome (1%). Twenty-seven deaths have been noted during the first year of dialysis treatment. The leading causes of death were cardio-vascular events (66, 67%), infection (22, 22%) and malignancy (11, 11%), The most common cardiovascular events were myocardial infarction (27.8%), sudden cardiac death (SCD) (27.8%) and heart failure (22.2%). CONCLUSION: In conclusion, our study showed that the main risk factors for ESRD patients in Aswan University Hospital are hypertensive nephrosclerosis, diabetic nephropathy, glomerulonephritis and idiopathic etiology, and the main causes of first-year mortality were cardiovascular events followed by infection and malignancy.

Melatonin ameliorates oxidative stress, modulates death receptor pathway proteins, and protects the rat cerebrum against bisphenol-A-induced apoptosis.

Epidemiological reports have indicated a correlation between the increasing of bisphenol-A (BPA) levels in the environment and the incidence of neurodegenerative diseases. In the present study, the protective effect of melatonin on oxidative stress and the death receptor apoptotic proteins in the cerebrum of the bisphenol-A-treated rats were examined. Adult male rats were orally administered melatonin (10mg/kg bw) concurrently with BPA (50mg/kg bw) 3 days a week for 6 weeks. BPA exposure resulted in significant elevations of oxidative stress, as evidenced by the increased malondialdehyde level and the decreased glutathione level and superoxide dismutase activity in the cerebrum. BPA caused an upregulation of p53 and CD95-Fas and activation of capsases-3 and 8, resulting in cerebral cell apoptosis. Melatonin significantly attenuated the BPA-evoked brain oxidative stress, modulated apoptotic-regulating proteins and protected against apoptosis. These data suggest that melatonin modulated important steps in the death receptor apoptotic pathway which likely related to its redox control properties. Melatonin is a promising pharmacological agent for preventing the potential neurotoxicity of BPA following occupational or environmental exposures.

Alfa-lipoic acid protects testosterone secretion pathway and sperm quality against 4-tert-octylphenol induced reproductive toxicity.

The protective effect of α-lipoic acid (LA) (50 mg/kg bw) against 4-tert-octylphenol (OP) (50 mg/kg bw) induced reproductive toxicity in male rats was studied. LA was injected 1h prior to OP administration three times a week. OP caused significant increase in oxidative stress in hypothalamus and epididymal sperm, disturbed hormonal levels in serum, decreased sperm quality, increased DNA fragmentation and loss of 35 and 95 kDa proteins in sperm, as well as elevated proliferating index in testis. LA protected against oxidative stress through promoting the levels of glutathione and glutathione-S-transferase in hypothalamus and sperm. In addition, LA prevented the decrease in testosterone, dehydroepiandrosterone sulfate, 3ß-hydroxysteroid dehydrogenase, and inhibited the elevations in sex-hormone-binding globulin levels and showed normal sperm quality. LA modulated proliferation of germ cell, protected against DNA fragmentation and maintained membrane protein organization in the sperm. In conclusion, LA normalized oxidative stress and protected testosterone synthesis pathway across hypothalamus-testicular axis and sperm quality indicating its defensive influence against OP-induced oxidative reproductive dysfunction in male rats.