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Hazim Abdulkarim Khatib,1 Waleed Ahmed Alghamdi,2 Ahmed Hussein Subki,3 Nadeem Shafique Butt,4 Mohammed Saad Alsallum,5 Ahmed Salem Alsulaimani,6 Sara Faisal Alnajjar,7 Fahad Daifallah Alzaidi,8 Abdulrahman Ali Alasmari,9 Hussein Mesfer Alshamrani,10 Faten Al-Zaben,2 Harold G Koenig2,11,12 1Department of Internal Medicine, King Abdulaziz Hospital, Jeddah, Saudi Arabia; 2Department of Psychiatry, King Abdulaziz University, Jeddah, Saudi Arabia; 3Department of Internal Medicine, King Faisal Specialist Hospital & Research Centre, Jeddah, Saudi Arabia; 4Department of Community Medicine, King Abdulaziz University, Jeddah, Saudi Arabia; 5Department of Neurology, King Abdulaziz Medical City, Jeddah, Saudi Arabia; 6Department of Emergency Medicine, King Fahad Medical City, Riyadh, Saudi Arabia; 7Department of Diagnostic Radiology, King Abdulaziz University Hospital, Jeddah, Saudi Arabia; 8Department of Internal Medicine, King Abdulaziz University Hospital, Jeddah, Saudi Arabia; 9Department of Forensic Medicine, Forensic Medicine Center, Jeddah, Saudi Arabia; 10Department of Dermatology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia; 11School of Public Health, Ningxia Medical University, Yinchuan, People’s Republic of China; 12Department of Psychiatry, Duke University Medical Center, Durham, NC, USACorrespondence: Waleed Ahmed Alghamdi; Harold G Koenig, Email wagalghamdi@kau.edu.sa; harold.koenig@duke.eduIntroduction: Skin Picking Disorder (SPD) is a skin-related disease, also recognized as psychogenic excoriation, dermatillomania, or excoriation disorder. SPD is defined as a habitual picking of skin, which in turn harms skin tissue. Given the paucity of information on SPD symptoms, their prevalence, and risk factors in Saudi Arabia, the present study seeks to fill this gap by investigating these factors in a community sample from Jeddah.Methods: This descriptive cross-sectional study was conducted in the city of Jeddah. The Skin Picking Scale-Re

Waleed Ahmed Alghamdi,1 Ahmed Hussein Subki,2 Hazim Abdulkarim Khatib,3 Nadeem Shafique Butt,4 Rahaf Ali Alghamdi,1 Mohammed Saad Alsallum,5 Ahmed A Alharbi,1 Mohammad Nasser Almatrafi,1 Abdullah Ahmed Alobisi,1 Faten Al-Zaben,1 Harold G Koenig1,6,7 1Department of Psychiatry, King Abdulaziz University, Jeddah, Saudi Arabia; 2Department of Internal Medicine, King Faisal Specialist Hospital & Research center, Jeddah, Saudi Arabia; 3Department of Internal Medicine, King Abdulaziz Hospital, Jeddah, Saudi Arabia; 4Department of Community Medicine, King Abdulaziz University, Jeddah, Saudi Arabia; 5Department of Neurology, King Abdulaziz Medical City, Jeddah, Saudi Arabia; 6School of Public Health, Ningxia Medical University, Yinchuan, People’s Republic of China; 7Duke University Medical Center, Durham, NC, USACorrespondence: Waleed Ahmed Alghamdi; Harold G Koenig, Email wagalghamdi@kau.edu.sa; harold.koenig@duke.eduBackground: The present study examined the prevalence of and risk factors for symptoms of body dysmorphic disorder (BDD) in the general population of Jeddah, a large port city in Saudi Arabia.Methods: This cross-sectional study surveyed a convenience sample of 520 adults. We used a validated self-screening measure to assess BDD, the body dysmorphic disorder questionnaire (BDDQ).Results: The prevalence of significant BDD symptoms among the general Saudi population was 8.8% (ie, those scoring above the cut off for BDD on the BDDQ). Over half (52%) of all respondents reported concerns about the attractiveness of their body parts, and of those expressing such concerns, 66% were preoccupied with these thoughts. Only 3% of all respondents opted for cosmetic surgery because of these concerns, and most of those individuals (69%) had only one surgery. Nearly 9% of all respondents reported that these concerns affected their relationships with family and friends. Almost 15% of all participants spent an hour or more each day thinking about these concerns. Patients wh

Ahmed Hussein Subki,1 Mohammed Ali Almalki,2 Nadeem Shafique Butt,3 Mohammed Saad Alsallum,4 Hatim Mashan Almutairi,5 Hazim Abdulkarim Khatib,6 Abdulrahman Mousa Alzahrani,6 Abdullah Salem Babaker,6 Firas Abdulrahman Addas,6 Abdullah Abdulfattah Mashat,7 Ammar Yasser Jad,6 Zohair Abdulwahab Zafar,6 Baraa Waleed Nogali,6 Abdulaziz Abdulsalam Alghamdi,6 Nasser Adel Alghamdi,6 Mohanad Fahad Dakhakhni,6 Omar Tamer Asaad,6 Kamal Waheeb Alghalayini6 1Department of Internal Medicine, King Faisal Specialist Hospital and Research Centre, Jeddah, Saudi Arabia; 2Department of Internal Medicine, King Faisal Medical Complex, Taif, Saudi Arabia; 3Department of Biostatistics, King Abdulaziz University, Jeddah, Saudi Arabia; 4Department of Neurology, King Abdulaziz Medical City, Jeddah, Saudi Arabia; 5Department of Radiology, Prince Mohammed Bin Abdulaziz Hospital, Riyadh, Saudi Arabia; 6Department of Internal Medicine, College of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia; 7Department of Surgery, College of Medicine, King Abdulaziz University, Jeddah, Saudi ArabiaCorrespondence: Kamal Waheeb AlghalayiniDepartment of Internal Medicine,College of Medicine, King Abdulaziz University, Jeddah, Saudi ArabiaTel +966-12-6408222 ext 18244-18272Email kalghalayini@kau.edu.saIntroduction: Heart failure (HF) affects about 320,000 Saudi individuals and is associated with a considerable negative impact on the patients’ quality of life. In literature, there is a lack of data about the echocardiographic abnormalities of HF patients in Saudi Arabia.Aim of Work: To describe the echocardiographic findings of HF patients in Western Saudi Arabia.Methodology: This was a retrospective record review study conducted on 2000 patients with chronic HF in Saudi Arabia. Demographic, clinical and echocardiographic data were collected and compared among patients with HF with reduced ejection fraction (HFrEF), ie, EF≤ 40%; HF with mid-range EF (HFmrEF), ie, EF=41– 49%; and

Renal proximal tubular cells constantly recycle nutrients to ensure minimal loss of vital substrates into the urine. Although most of the transport mechanisms have been discovered at the molecular level, little is known about the factors regulating these processes. Here, we show that mTORC1 and mTORC2 specifically and synergistically regulate PTC endocytosis and transport processes. Using a conditional mouse genetic approach to disable nonredundant subunits of mTORC1, mTORC2, or both, we showed that mice lacking mTORC1 or mTORC1/mTORC2 but not mTORC2 alone develop a Fanconi-like syndrome of glucosuria, phosphaturia, aminoaciduria, low molecular weight proteinuria, and albuminuria. Interestingly, proteomics and phosphoproteomics of freshly isolated kidney cortex identified either reduced expression or loss of phosphorylation at critical residues of different classes of specific transport proteins. Functionally, this resulted in reduced nutrient transport and a profound perturbation of the endocytic machinery, despite preserved absolute expression of the main scavenger receptors, MEGALIN and CUBILIN. Our findings highlight a novel mTOR-dependent regulatory network for nutrient transport in renal proximal tubular cells.

Renal proximal tubular cells constantly recycle nutrients to ensure minimal loss of vital substrates into the urine. Although most of the transport mechanisms have been discovered at the molecular level, little is known about the factors regulating these processes. Here, we show that mTORC1 and mTORC2 specifically and synergistically regulate PTC endocytosis and transport processes. Using a conditional mouse genetic approach to disable nonredundant subunits of mTORC1, mTORC2, or both, we showed that mice lacking mTORC1 or mTORC1/mTORC2 but not mTORC2 alone develop a Fanconi-like syndrome of glucosuria, phosphaturia, aminoaciduria, low molecular weight proteinuria, and albuminuria. Interestingly, proteomics and phosphoproteomics of freshly isolated kidney cortex identified either reduced expression or loss of phosphorylation at critical residues of different classes of specific transport proteins. Functionally, this resulted in reduced nutrient transport and a profound perturbation of the endocytic machinery, despite preserved absolute expression of the main scavenger receptors, MEGALIN and CUBILIN. Our findings highlight a novel mTOR–dependent regulatory network for nutrient transport in renal proximal tubular cells.

Renal proximal tubular cells constantly recycle nutrients to ensure minimal loss of vital substrates into the urine. Although most of the transport mechanisms have been discovered at the molecular level, little is known about the factors regulating these processes. Here, we show that mTORC1 and mTORC2 specifically and synergistically regulate PTC endocytosis and transport processes. Using a conditional mouse genetic approach to disable nonredundant subunits of mTORC1, mTORC2, or both, we showed that mice lacking mTORC1 or mTORC1/mTORC2 but not mTORC2 alone develop a Fanconi-like syndrome of glucosuria, phosphaturia, aminoaciduria, low molecular weight proteinuria, and albuminuria. Interestingly, proteomics and phosphoproteomics of freshly isolated kidney cortex identified either reduced expression or loss of phosphorylation at critical residues of different classes of specific transport proteins. Functionally, this resulted in reduced nutrient transport and a profound perturbation of the endocytic machinery, despite preserved absolute expression of the main scavenger receptors, MEGALIN and CUBILIN. Our findings highlight a novel mTOR–dependent regulatory network for nutrient transport in renal proximal tubular cells.