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Salivary glands are greatly responsible for maintaining oral tissue homeostasis by the secretion of saliva. This study was designed to investigate the changes of aquaporin 1 and 4, oxidative stress and autophagy in submandibular and parotid salivary glands of diabetic rats and the possible ameliorative effect of intermittent fasting on these changes. Fifty adult male rats were divided into control and experimental groups. Experimental diabetes was induced by a single intraperitoneal injection of streptozotocin. After diabetic induction, the experimental group was divided into two groups (diabetic without intermittent fasting and diabetic with intermittent fasting). Animals were sacrificed two and four weeks after induction of diabetes. Intermittent fasting significantly decreased malondialdehyde and significantly elevated reduced glutathione (GSH) in the submandibular and parotid glands compared to those in diabetic rats. The salivary secretions were also significantly spared histologically in diabetics with intermittent fasting groups. As well, intermittent fasting up-regulated aquaporin 1 in both glands, while aquaporin 4 was only elevated in submandibular gland. Immunolocalization and gene expression of Lc3-II was higher in diabetic salivary glands than in fasting glands. In conclusion, these findings highlight the pathological role of autophagy in diabetic sub-mandibular and parotid glands and provide potential target for therapeutic role of intermittent fasting to ameliorate submandibular and parotid glands dysfunction in type I diabetes mellitus.

Cryptorchidism causes spermatogenic failure and reduced serum androgen levels, as well as testicular oedema and fibrosis, which are hallmarks of inflammation. However, the role of inflammation and the effects of cryptorchidism on Sertoli cell and Leydig cell function at the molecular level remain ill-defined. Bilateral cryptorchidism was surgically induced in adult rats for 7 and 14 weeks. Testis weights decreased to 40% of normal within 7 weeks, due to loss of all developing spermatogenic cells except spermatogonia, but did not decrease further at 14 weeks. Serum FSH and LH were increased at both time points, consistent with a loss of feedback by inhibin and testosterone. This damage was accompanied by progressive accumulation of interstitial fluid and peritubular fibrosis, and a progressive decline of several critical Sertoli cell genes (Sox9, Inha (inhbin α-subunit), Cldn11 (claudin 11), Gja1 (connexin 43), and Il1a (interleukin-1α)) and the Leydig cell steroidogenic enzymes, Cyp11a1, Hsd3b1, and Hs17b3. Activin B and the activin-binding protein, follistatin, also declined, but the intratesticular concentration of activin A, which is a regulator of inflammatory responses, was largely unaffected at either time point. Expression of genes involved in inflammation (Tnf, Il10, Il1b, Mcp1) and fibrosis (Acta2, Col1a1) were considerably elevated at both time points. These data indicate that induction of experimental cryptorchidism, which causes complete failure of spermatogenesis in the adult rat, also induces chronic testicular inflammation, manifesting in oedema and fibrosis, and a progressive decline of Sertoli and Leydig cell gene expression and function.

A body of literature supports the postulation that a persistent lipid metabolic imbalance causes lipotoxicity, "an abnormal fat storage in the peripheral organs". Hence, lipotoxicity could somewhat explain the process of sarcopenia, an aging-related, gradual, and involuntary decline in skeletal muscle strength and mass associated with several health complications. This review focuses on the recent mechanisms underlying lipotoxicity-related sarcopenia. A vicious cycle occurs between sarcopenia and ectopic fat storage via a complex interplay of mitochondrial dysfunction, pro-inflammatory cytokine production, oxidative stress, collagen deposition, extracellular matrix remodeling, and life habits. The repercussions of lipotoxicity exacerbation of sarcopenia can include increased disability, morbidity, and mortality. This suggests that appropriate lipotoxicity management should be considered the primary target for the prevention and/or treatment of chronic musculoskeletal and other aging-related disorders. Further advanced research is needed to understand the molecular details of lipotoxicity and its consequences for sarcopenia and sarcopenia-related comorbidities.

The deltoid ligament (DL) is a strong triangle-shaped ligament with a complex fascicular arrangement. Understanding the morphological and/or functional typing of the DL structure is hindered by a paucity of clear, quantitative, and reproducible data and is further complicated by inconsistent terminology use. The aim of this work was to describe different components of the DL using strict identification criteria.Thirty embalmed cadaveric ankles of both sides were dissected on all sides and studied by using gross examination, micro-dissection, and light microscopy by tracing the fascicular pattern of each under 6X magnification.Six ligamentous bands were identified. The tibiotalocalcaneal ligament (TTC) and the superficial posterior tibiotalar ligament (sPTT) were two superficial variants and the anterior tibiotalar ligament (ATT), the anterior tibiotalonavicular ligament (ATTN), the intermediate tibiotalar ligament (ITT), and the deep posterior tibiotalar ligament (dPTT) were four deep variants. The TTC was identified in all 30 embalmed cadaveric specimens. Five additional ligamentous bands (ITT, sPTT, dPTT, ATT, and ATTN) were variable findings in the current cohort.This study presents six ligamentous bands as a regular finding and five additional ligamentous bands as variable findings in the dissected specimen. This data could assist in the radiological diagnosis of DL injuries and advanced procedures related to its surgical repair and reconstruction.

Background: The area of the cubital fossa contains the main superficial veins, including the basilic, cephalic, median cubital, and median antebrachial veins, and their innominate small tributaries. For this reason, it is the area most preferred by medical practitioners to access the circulatory system for various clinical applications. Objective: The aim of this study was to address the prevalence of different types of antecubital fossa superficial vein patterns observable among Saudi subjects by applying a tourniquet and using a VeinViewer®. Materials and methods: Over the period from September 2020 to April 2021, a cross-sectional study was carried out in the Eastern Province of Saudi Arabia. The 151 study subjects were randomly chosen from the emergency department of King Fahad University Hospital. A total of 302 venous patterns were obtained; 55 were excluded due to the presence of scar tissues over the antecubital fossa, obesity, or thick subcutaneous tissue. Four classes of cubital venous patterns were established according to other studies, and a VeinViewer® and a tourniquet were used to visualize the venous patterns. Results: Of the 151 people, 21 were female and 130 were male. Among the included 247 venous patterns, the predominant type was type 2 (52.2%), characterized by a branching off the median cubital vein from the cephalic vein and an upward progression to join the basilic vein. Conclusion: Type 2 appears to be the dominant pattern, with no significant relation to the origins of the parents, in the Saudi population. Gender does not influence the venous patterns. Further studies are needed outside the restrictions of the COVID-19 pandemic to obtain a larger sample.

Cryptorchidism causes spermatogenic failure and reduced serum androgen levels, as well as testicular oedema and fibrosis, which are hallmarks of inflammation. However, the role of inflammation and the effects of cryptorchidism on Sertoli cell and Leydig cell function at the molecular level remain ill-defined. Bilateral cryptorchidism was surgically induced in adult rats for 7 and 14 weeks. Testis weights decreased to 40% of normal within 7 weeks, due to loss of all developing spermatogenic cells except spermatogonia, but did not decrease further at 14 weeks. Serum FSH and LH were increased at both time points, consistent with a loss of feedback by inhibin and testosterone. This damage was accompanied by progressive accumulation of interstitial fluid and peritubular fibrosis, and a progressive decline of several critical Sertoli cell genes (Sox9, Inha (inhbin α-subunit), Cldn11 (claudin 11), Gja1 (connexin 43), and Il1a (interleukin-1α)) and the Leydig cell steroidogenic enzymes, Cyp11a1, Hsd3b1, and Hs17b3. Activin B and the activin-binding protein, follistatin, also declined, but the intratesticular concentration of activin A, which is a regulator of inflammatory responses, was largely unaffected at either time point. Expression of genes involved in inflammation (Tnf, Il10, Il1b, Mcp1) and fibrosis (Acta2, Col1a1) were considerably elevated at both time points. These data indicate that induction of experimental cryptorchidism, which causes complete failure of spermatogenesis in the adult rat, also induces chronic testicular inflammation, manifesting in oedema and fibrosis, and a progressive decline of Sertoli and Leydig cell gene expression and function.

The testis is a temperature-sensitive organ that needs to be maintained 2–7 °C below core body temperature to ensure the production of normal sperm. Failure to maintain testicular temperature in mammals impairs spermatogenesis and leads to low sperm counts, poor sperm motility and abnormal sperm morphology in the ejaculate. This review discusses the recent knowledge on the response of testicular somatic cells to heat stress and, specifically, regarding the relevant contributions of heat, germ cell depletion and inflammatory reactions on the functions of Sertoli and Leydig cells. It also outlines mechanisms of testicular thermoregulation, as well as the thermogenic factors that impact testicular function.

Heat reversibly disrupts spermatogenesis, but the effects on Sertoli cell (SC) function and inhibin/activin-related proteins are less well-defined. Adult rat testis weights decreased by 40% within 2 weeks after heat-treatment (43 °C, 15 min), due to loss of pachytene spermatocytes and round spermatids. Coincident effects were reduced SC nuclear volume at one week and >50% reduction in expression of several critical SC genes (Inha, Cld11, Gja1, Tjp1, Cldn3) by 2 weeks. Leydig cell steroidogenic enzymes, Cyp11a1, Hsd3b1, were also reduced. Activin gene expression was unaffected at this time, but expression of the activin-binding protein, follistatin (Fst), increased >2-fold. At 4–8 weeks, coincident with the recovery of spermatocytes and early spermatids, but progressive loss of elongated spermatids, most SC genes had recovered; however, testicular activin A was reduced and activin B increased. At 8 weeks, serum inhibin was decreased and, consequently, serum FSH increased. Crucially, germ cell damage was not associated with a significant inflammatory response. At 14 weeks, most testicular parameters had returned to normal, but testis weights remained slightly reduced. These data indicate that, following acute heat-treatment, expression of several key Sertoli and Leydig cell genes declined in parallel with the initial loss of meiotic germ cells, whereas activins were responsive to the subsequent loss of mature spermatids, leading to an increase in testicular activin B production relative to activin A.