Topographic Anatomy of the Medial Labyrinthine Wall: Implications for the Transcanal Endoscopic Approach to the Internal Auditory Canal.

Hypothesis To characterize transcanal endoscopic landmarks of the medial labyrinthine wall and correlate these with anatomical features of the fundus of the internal auditory canal (IAC). Background The transcanal transpromontorial approach (TTA) enables minimally invasive access to the IAC. The establishment of a landmark-based dissection technique for the approach is crucial to avoid injury to the facial nerve. Methods Twenty temporal bones were dissected endoscopically through the TTA. Furthermore, high-resolution computed tomography (CT) scans from ten adult normal temporal bones were analyzed and three-dimensionally reconstructed. Results A stepwise dissection technique for the TTA was demonstrated depending on a newly described landmark used in the identification of the facial nerve. The proposed landmark, which was named the intervestibulocochlear crest (IVCC), is an integrated part of the otic capsule. It can be differentiated after the excision of the lateral labyrinthine wall as a laterally based bony pyramid between the cochlea and the vestibule. Its medially directed apex blends with the central part of the falcifrom crest and points to the distal part of the meatal facial nerve. The IVCC is best detected on axial CT images at the level of the tympanic facial nerve. The union between the IVCC and the falciform crest appears radiologically as a short stem or mini-martini glass. Conclusion The proposed IVCC is a novel landmark with a consistent relationship to the IAC fundus and the facial nerve. It may be utilized in conjunction with the falciform crest to identify the facial nerve during minimally invasive transcanal surgeries. METHODS Twenty temporal bones were dissected endoscopically through the TTA. Furthermore, high-resolution computed tomography (CT) scans from ten adult normal temporal bones were analyzed and three-dimensionally reconstructed. RESULTS A stepwise dissection technique for the TTA was demonstrated depending on a newly described landmark used in the identification of the facial nerve. The proposed landmark, which was named the intervestibulocochlear crest (IVCC), is an integrated part of the otic capsule. It can be differentiated after the excision of the lateral labyrinthine wall as a laterally based bony pyramid between the cochlea and the vestibule. Its medially directed apex blends with the central part of the falcifrom crest and points to the distal part of the meatal facial nerve. The IVCC is best detected on axial CT images at the level of the tympanic facial nerve. The union between the IVCC and the falciform crest appears radiologically as a short stem or mini-martini glass. CONCLUSION The proposed IVCC is a novel landmark with a consistent relationship to the IAC fundus and the facial nerve. It may be utilized in conjunction with the falciform crest to identify the facial nerve during minimally invasive transcanal surgeries

Characterization of greater middle eastern genetic variation for enhanced disease gene discovery

The Greater Middle East (GME) has been a central hub of human migration and population admixture. The tradition of consanguinity, variably practiced in the Persian Gulf region, North Africa, and Central Asia1-3, has resulted in an elevated burden of recessive disease4. Here we generated a whole-exome GME variome from 1,111 unrelated subjects. We detected substantial diversity and admixture in continental and subregional populations, corresponding to several ancient founder populations with little evidence of bottlenecks. Measured consanguinity rates were an order of magnitude above those in other sampled populations, and the GME population exhibited an increased burden of runs of homozygosity (ROHs) but showed no evidence for reduced burden of deleterious variation due to classically theorized ‘genetic purging’. Applying this database to unsolved recessive conditions in the GME population reduced the number of potential disease-causing variants by four- to sevenfold. These results show variegated genetic architecture in GME populations and support future human genetic discoveries in Mendelian and population genetics

Pioglitazone versus metformin in two rat models of glucose intolerance and diabetes

Insulin resistance has been implicated in the pathogenesis of type 2 diabetes. High fat diets cause insulin resistance. Both metformin and pioglitazone are considered "insulin sensitizers" and used as antihyperglycemic agents for type 2 diabetes treatment. The aim of this study is to Compare pioglitazone and metformin effects on carbohydrate metabolism and insulin sensitivity in diabetic and glucose intolerant rats on high fat diet. Male albino rats were randomized to seven groups. The 1st group received high carbohydrate diet (control). The 2nd, 3rd and 4th groups received high sunflower oil diets for 6 weeks and either left untreated, or given pioglitazone or metformin during the last 3 weeks. The 5th, 6th, and 7th groups were made diabetic by STZ injection on day 15 of the 6 weeks-high fat diet regimen. They were either left untreated, or given pioglitazone or metformin during the last 3 weeks. High-fat diet induced glucose intolerance; represented by increase of serum glucose associated with increase in liver glucose-6-phosphatase and decreases in liver glucose-6-phosphate dehydrogenase and glucokinase activities. No significant differences were observed between pioglitazone and metformin. In diabetic rats, both pioglitazone and metformin decreased elevated serum glucose by ~30%. Only metformin increased hepatic glycogen, and normalized glucose-6-phosphatase activity. On the other hand, pioglitazone normalized elevated renal glycogen content and increased glucose-6-phosphate dehydrogenase activity. High sunflower oil diet impaired glucose tolerance. Pioglitazone and metformin had comparable effects on estimates of carbohydrate metabolism and insulin sensitivity in high-fat fed rats, but different effects in diabetic rats

Internet of Things: A Comprehensive Overview on Protocols, Architectures, Technologies, Simulation Tools, and Future Directions

The Internet of Things (IoT) is a global network of interconnected computing, sensing, and networking devices that can exchange data and information via various network protocols. It can connect numerous smart devices thanks to recent advances in wired, wireless, and hybrid technologies. Lightweight IoT protocols can compensate for IoT devices with restricted hardware characteristics in terms of storage, Central Processing Unit (CPU), energy, etc. Hence, it is critical to identify the optimal communication protocol for system architects. This necessitates an evaluation of next-generation networks with improved characteristics for connectivity. This paper highlights significant wireless and wired IoT technologies and their applications, offering a new categorization for conventional IoT network protocols. It provides an in-depth analysis of IoT communication protocols with detailed technical information about their stacks, limitations, and applications. The study further compares industrial IoT-compliant devices and software simulation tools. Finally, the study provides a summary of the current challenges, along with a broad overview of the future directions to tackle the challenges, in the next IoT generation. This study aims to provide a comprehensive primer on IoT concepts, protocols, and future insights that academics and professionals can use in various contexts

Rheumatological manifestations in patients with malignancies: Relation to immune modulation therapy

Background: The relation between malignancies and rheumatic diseases (RDs) is complex with commonly shared symptoms. Rheumatological manifestations of malignancies may present as paraneoplastic syndromes and could follow chemotherapy. Aim of the work: to investigate rheumatic manifestations of patients with hematologic or solid malignancies and the relation to immune-modulation therapy. Patients and methods: The study included 25 patients with hematological and another 25 with solid malignancies. Patients were subjected to medical history, recording medications received, musculoskeletal examination and laboratory assessment. Results: The mean age and F:M of patients with hematological (43.7 ± 16.04 y and F:M 1.5:1) was significantly lower than those with solid (53.6 ± 14.3 y and F:M 7.3:1) malignancies (p = 0.025 and p = 0.024). Rheumatological manifestations as the first presentation was significantly higher in patients with haematological (60%) compared to solid (20%) malignancies (p = 0.004). Articular involvement was the commonest rheumatological manifestation (72%) followed by mucocutaneous (18%), oral/genital ulcers (10%), thromboembolic events (10%), Raynauds (8%), dry eyes (8%), myositis (6%) and myalgia (4%). The total leucocytic count and serum uric acid were significantly lower in patients with solid tumors (p = 0.045 and p = 0.026 respectively) and autoimmune markers were similar. Dry eye (16.7%), oral/genital ulcers (20.8%) and Raynaud‘s (16.7%) was present only in patients receiving anti-cancer treatment (n = 24). Paradoxically, arthritis was more frequent in those not receiving chemotherapy (n = 17) while myalgia (25%) was evident in those receiving checkpoint inhibitors (n = 8). Conclusion: Rheumatological manifestations occur with solid and hematological malignancies before or throughout the disease course and the most frequent was articular. Myalgia was associated with checkpoint inhibitors

Blood Ammonia Level Correlates with Severity of Cirrhotic Portal Hypertensive Gastropathy

Background. Portal hypertensive gastropathy (PHG) is a common anomaly with potential for bleeding found in portal hypertension. Blood ammonia levels correlate well with liver disease severity and existence of portosystemic shunts. Increased ammonia results in vasodilation and hepatic stellate cell activation causing and exacerbating portal hypertension. Objective. To assess the relation of blood ammonia to the presence and severity of portal hypertensive gastropathy in cirrhosis. Methods. This cross-sectional study included 381 cirrhotics undergoing screening for esophageal varices (EV) divided into a portal hypertensive gastropathy group (203 patients with EV and PHG), esophageal varix group (41 patients with EV but no PHG), and control group (137 patients with no EV or PHG). A full clinical examination, routine laboratory tests, abdominal ultrasonography, child score calculation, and blood ammonia measurement were performed for all patients. Results. Blood ammonia, portal vein, splenic vein, and splenic longitudinal diameters were significantly higher and platelet counts lower in patients with EV and EV with PHG than controls. Patients having EV with PHG had significantly higher bilirubin and ammonia than those with EV but no PHG. Severe PHG was associated with significantly higher ammonia, EV grades, and superior location and a lower splenic longitudinal diameter than mild PHG. The PHG score showed a positive correlation with blood ammonia and a negative correlation with splenic longitudinal diameter. Conclusions. Blood ammonia levels correlate with the presence, severity, and score of portal hypertensive gastropathy in cirrhosis suggesting a causal relationship and encouraging trials of ammonia-lowering treatments for the management of severe PHG with a tendency to bleed

Pilot study of classic galactosemia: Neurodevelopmental impact and other complications urge neonatal screening in Egypt

Classic galactosemia is caused by deficiency of galactose-1-phosphate uridylyltransferase (GALT). It causes serious morbidity and mortality if left untreated. Screening for galactosemia is not included in Egyptian neonatal screening program. The study aimed to define clinical presentation and complications of galactosemia at Pediatric Hepatology Clinic, Cairo University, Egypt. Thus, the clinical presentation, course and outcome of 37 children with documented galactosemia was studied. Jaundice was the main presentation (67.6%). Other presentations included; convulsions (29.7%), motor retardation (24.3%), mental retardation (5.4%), microcephaly (5.4%), failure to thrive (16.2%), hepatomegaly (62.2%), splenomegaly (35.1%), vomiting (16.2%), diarrhea (8.1%), liver cell failure (10.8%), renal tubular acidosis (5.4%), cataract (5.4%), autoimmune hepatitis (2.7%), self-mutilation (2.7%), combined immune deficiency (2.7%) and kernicterus (2.7%). There was no correlation of residual enzyme activity to severity, clinical presentation, liver function tests, liver biopsy findings or outcome apart from highly significant correlation with repeated chest infections (P = 0.001). Duration to diagnosis and exposure to galactose in diet correlated with liver pathology severity i.e. hepatocyte necrosis (P = 0.003) and cytoskeleton damage (P = 0.003), but not to outcome. Galactosemia should be suspected in any child with liver, neurologic disease and/or immunodeficiency. Its complications are potentially preventable. Early detection is mandatory to prevent serious morbidity and mortality. Initiation of neonatal screening for galactosemia in Egypt is recommended. Keywords: Classic galactosemia, Galactose-1-phosphate uridylyltransferase GALT, Convulsions motor retardation mental retardation, Kernicterus microcephaly, Liver cell failure autoimmune hepatitis, Cataract self-mutilation combined immune deficienc