The Klippel-Trenaunay syndrome is a combination of venous and capillary malformations associated with soft tissue and/or bony limb hypertrophy, with or without lymphatic malformations. Although persistent foetal veins are rare, the persistence of the lateral marginal vein is a common association in this syndrome. It results in venous hypertension, which gives rise to venous varicosities, which are commonly seen in this syndrome. This is a case report of a 28-year-old man with Klippel-Trenaunay syndrome, with persistence of the lateral marginal vein, affecting his right lower limb. He was treated with an above-knee amputation. The amputated limb was dissected to demonstrate the anatomy of the lateral marginal vein. To the best of the authors' knowledge, the gross anatomy of the lateral marginal vein has not been previously reported.
Hypertrophy of the inferior turbinates are the major cause of nasal obstruction. CO2 lasers have been used to reduce the size of the inferior turbinates over the last 20 years. However, the many techniques of delivery of the laser show that there is no one standard method reducing the size of the turbinates. We now describe how the laser can be applied directly to the turbinates using a handpiece with a special nasal tip, thus overcoming the disadvantages delivery via arthroscopic devices, microscopes and fibers. This technique is further enhanced by coupling it with Swiftlase which swirls the focused beam in a 3 mm spot thus ablating tissue more quickly. This procedure is done under local anaesthesia. The ablation of the anterior third of the inferior turbinates effectively overcomes nasal obstruction. This new method was compared to the more traditional submucus diathermy. 22 patients were subjected to laser treatment whilst 20 patients were subjected to diathermy. The outcome was evaluated subjectively by the patients themselves at 2 weeks, 3 months and 6 months. At the end of the study, the laser group reported a more significantly improved nasal airway (91% against 75%) and decreased rhinorrhea (72.7% against 35%) when compared to the diathermy group.
A small amount of Methamphetamine (MA) can produce behavioural changes such as euphoria, increased alertness, paranoia, decreased appetite and increased physical activity. In cardiovascular system, it can produce chest pain and hypertension which can result in cardiovascular collapse. In addition, MA causes accelerated heartbeat, elevated blood pressure. It can also cause irreversible damage to blood vessels in the brain. A number of sympathomimetic amines are capable of causing myocardial damage, but the cardio-toxic action of MA has been of particular interest since standardized dosage consistently produces myocardial lesions. As this drug is a choice of many teenagers and young adults, the damage to their health, as well as their future aspects could be greatly affected, therefore more evidence must be sought to convince them the negative root and show them the optimism of recovery and salvation. To clarify the effect of Methamphetamine (MA) on myocardium, 56 male Wister rats aged four weeks were divided equally into MA, Methamphetamine withdrawal (MW), Placebo (P) and Control (C) group were examined following daily intra-peritoneal administration of MA at a dose of 5 mg/kg body weight for 2, 4, 8 and 12 weeks. Normal saline was similarly injected in P group. Light microscopic changes was seen in the myocardium of MA treated group including eosinophilic degeneration, atrophy, hypertrophy, disarray, edema, cellular infiltration, myolysis, granulation tissue, fibrosis and vacuolization. On the other hand, the withdrawal group showed evidence of gradual recovery of those myocardial changes. Optimism is therefore generated about possibility of returning towards normal by withdrawing of this drug by the addicts.
Rutin is a flavonoid with antioxidant property. It has been shown to exert cardioprotection against cardiomyocyte hypertrophy. However, studies regarding its antihypertrophic property are still lacking, whether it demonstrates similar antihypertrophic effect to its metabolite, quercetin. Hence, this study aimed to investigate the effects of both flavonoids on oxidative stress and mitogen-activated protein kinase (MAPK) pathway in H9c2 cardiomyocytes that were exposed to angiotensin II (Ang II) to induce hypertrophy. Cardiomyocytes were exposed to Ang II (600 nM) with or without quercetin (331 μM) or rutin (50 μM) for 24 h. A group given vehicle served as the control. The concentration of the flavonoids was chosen based on the reported effective concentration to reduce cell hypertrophy or cardiac injury in H9c2 cells. Exposure to Ang II increased cell surface area, intracellular superoxide anion level, NADPH oxidase and inducible nitric oxide synthase activities, and reduced cellular superoxide dismutase activity and nitrite level, which were similarly reversed by both rutin and quercetin. Rutin had no significant effects on phosphorylated proteins of extracellular signal-related kinases (ERK1/2) and p38 but downregulated phosphorylated c-Jun N-terminal kinases (JNK1/2), which were induced by Ang II. Quercetin, on the other hand, had significantly downregulated the phosphorylated proteins of ERK1/2, p38, and JNK1/2. The quercetin inhibitory effect on JNK1/2 was stronger than the rutin. In conclusion, both flavonoids afford similar protective effects against Ang II-induced cardiomyocyte hypertrophy, but they differently modulate MAPK pathway.