Investigation of Obesity-Related HAdV-36 in NAFLD Patients: a Case-Control Study.

BACKGROUND: HAdV-36 leads to adipocyte proliferation of adipose tissue through E4orf1 gene, leading to the development of obesity and related diseases. We aimed to investigate the presence and any association of HAdV-36 in non-alcoholic fatty liver disease (NAFLD) patients Methods: The patient group was composed of 116 patients; 30 obese patients with NAFLD (BMI > 30 kg/m2), 30 patients with Diabetes Mellitus (DM)+NAFLD (BMI > 30 kg/m2), 16 patients with NAFLD (BMI < 30 kg/m2), and operated obese group with NAFLD (BMI > 30 kg/m2). The control group comprised 81 non-obese healthy adults. Liver adipose tissue samples were obtained in 30 operated NAFLD patients. HAdV-36-DNA, HAdV-36 neutralizing antibodies, serum lipid, and adipokine levels were analyzed. RESULTS: HAdV-36 neutralizing antibodies (HAdV-36 Ab-positive) were detected in 10/116 and 2/81 participants in the study and control groups, respectively; the difference was statistically significant (p < 0.005). LDL, total cholesterol but not adipokine levels were found to be significantly higher in HadV-36 Ab-positive patients (p < 0.05). While HAdV-36 was identified as a risk factor with OR = 4.11 in univariate analyses, there was no significant difference in binary logistic regression analysis. HAdV-36-DNA was detected in the adipose tissue samples of two patients. CONCLUSIONS: We suggest that the presence of HAdV-36 may lead to the development of obesity with the increase in adipose tissue, and diseases such as hyperlipidemia, NAFLD, DM, and metabolic syndrome may develop on the basis of chronic inflammation caused by obesity. Thus, HAdV-36 may be a plausible risk factor for the development of NAFLD.

Histomorphometric evaluation of the effect of systemic and topical ozone on alveolar bone healing following tooth extraction in rats.

The aim of this study was to investigate the effects of systemic and topical ozone applications on alveolar bone healing following tooth extraction. One hundred and twelve male Wistar rats were divided into eight groups of 14 rats each; seven groups were experimental (A-G) and one formed the control group (K). The experimental groups were further divided into two sub-groups, with seven rats in each - sacrificed on days 14 and 28 (subgroups 1 and 2). The maxillary right central incisors were extracted under general anaesthesia following the administration of local anaesthesia. After sacrifice, semi-serial histological sections were prepared, and mineralized and trabecular bone and osteoid and osteoblast surfaces were measured. Measurements of the trabecular bone showed statistically higher values in the groups treated with systemic ozone (D(2): 50.01 ± 2.12; E(2): 49.03 ± 3.03; F(2): 48.76 ± 2.61; G(2): 50.24 ± 3.37) than in the groups that underwent topical ozone administration (A(2): 46.01 ± 3.07; B(2): 46.79 ± 3.09; C(2): 47.07 ± 2.12; P = 0.030 (G(2)-A(2), G(2)-B(2), G(2)-C(2))). Within the limitations of the current study, it may be concluded that postoperative long-term systemic ozone application can accelerate alveolar bone healing following extraction. However, additional studies are required to clarify the effects of the different ozone applications on new bone formation.

Percutaneous transluminal angioplasty of the inferior right hepatic vein for the treatment of Budd-Chiari syndrome.

Budd-Chiari Syndrome is one of the several causes of portal hypertension and is characterised by hepatomegaly, ascites and abdominal pain. The treatment requires either medical or interventional/surgical procedures. A case of Budd-Chiari Syndrome with a membranous web that causes obstruction in the ostium of the inferior right hepatic vein is reported here which was treated by percutaneous transluminal angioplasty (PTA). The patient was asymptomatic and off medication and there was no recurrence after 18-months follow-up.

Atypical hemorrhagic bullous pyoderma gangrenosum.

A 55-year-old woman was seen in the Plastic and Reconstructive Surgery Clinic because of a nonhealing wound on her left leg of approximately 2 months' duration. She had an 8-month history of multiple wounds appearing on her arms and legs. The patient noted that the majority of the wounds had been treated and healed with the use of topical medications. One wound on her left leg had continued to enlarge rapidly despite topical treatments. Therefore, hyperbaric oxygen therapy had been administered for 15 sessions. No additional healing had occurred with this treatment. Skin grafting was performed on the affected area. She developed ulcers and blistering lesions at surgical and nonsurgical sites after skin grafting. The patient was referred to the Dermatology Department. Dermatologic examination revealed a deep, necrotic ulcer, 30 cm x 10 cm, with surrounding violaceous erythema on the donor area, ulceration (18 cm x 8 cm) on the graft area, a hemorrhagic bullous plaque (5 cm x 15 cm) over the right malleolus, scattered ecchymotic lesions and small hemorrhagic bullae on both legs, and small pustules around the staplers (Fig. 1a,b). Cutaneous biopsy of a new lesion revealed a focal, dense neutrophilic infiltrate, liquefaction degeneration in the center, lymphocytic and mild plasmacytic infiltration around the venules, and fibrinoid deposits in the walls and lumen of the vessels (Fig. 2a). In addition, excessive polymorphonuclear leukocytes and extravasated erythrocytes were present in the papillary and reticular dermis (Fig. 2b). The patient had a 14-year history of asthma bronchiale. Physical examination did not reveal any abnormality, except for crackling rales at the base of each lung. Laboratory examinations were within normal limits, except for the sedimentation rate (55 mm/h). Protein electrophoresis, peripheral blood smear, abdominal ultrasound, and thorax and abdominopelvic computed tomography scans were all normal. Swab cultures from the ulcers were negative. Bullous pyoderma gangrenosum was diagnosed on clinical and histopathologic grounds. Prednisolone 80 mg/day was started. Rapid epithelialization was observed within 2 months of treatment. The dose of prednisolone was gradually decreased to 20 mg/day, and was used as a maintenance dose for an additional 6 months. Complete improvement was achieved in 8 months. The patient has been followed up for approximately 1 year. There were no side effects observed during the treatment and in addition no new lesions developed at the follow-up.