• Journal of Trauma and Injury
• /
• v.37 no.2
• /
• pp.158-160
• /
• 2024

Arterial thoracic outlet syndrome (TOS) resulting from thoracic trauma is an exceedingly rare condition, typically caused by a fracture of the first rib or clavicle. In this report, the author presents a case of traumatic arterial TOS precipitated by multiple left rib fractures, notably excluding the first rib, following a fall from a 2-m high stepladder. The patient was treated successfully with first rib resection via a transaxillary approach, and the postoperative course was uneventful. The literature includes no known reports of traumatic arterial TOS in patients with multiple fractures that spare the first rib, making this the first documented case of its kind. In this instance, the patient sustained fractures to the fourth and fifth ribs. The TOS was likely not a direct result of the multiple rib fractures, which were located some distance from the thoracic outlet. Rather, it is hypothesized that the trauma from these fractures caused a soft tissue injury within the thoracic outlet, which ultimately led to the development of TOS.

• Biomolecules & Therapeutics
• /
• v.23 no.1
• /
• pp.19-25
• /
• 2015

Vascular endothelial growth factor (VEGF) is an important regulator of neovascularization. Hypoxia inducible nitric oxide (NO) enhanced the expression of VEGF and thymosin beta-4 ($T{\beta}4$), actin sequestering protein. Here, we investigated whether NO-mediated VEGF expression could be regulated by $T{\beta}4$ expression in HeLa cervical cancer cells. Hypoxia inducible NO production and VEGF expression were reduced by small interference (si) RNA of $T{\beta}4$. Hypoxia response element (HRE)-luciferase activity and VEGF expression were increased by the treatment with N-(${\beta}$-D-Glucopyranosyl)-N2-acetyl-S-nitroso-D, L-penicillaminamide (SNAP-1), to generate NO, which was inhibited by the inhibition of $T{\beta}4$ expression with $T{\beta}4$-siRNA. In hypoxic condition, HRE-luciferase activity and VEGF expression were inhibited by the treatment with $N^G$-monomethyl-L-arginine (L-NMMA), an inhibitor to nitric oxide synthase (NOS), which is accompanied with a decrease in $T{\beta}4$ expression. VEGF expression inhibited by L-NMMA treatment was restored by the transfection with pCMV-$T{\beta}4$ plasmids for $T{\beta}4$ overexpression. Taken together, these results suggest that $T{\beta}4$ could be a regulator for the expression of VEGF via the maintenance of NOS activity.

• Archives of Plastic Surgery
• /
• v.43 no.6
• /
• pp.491-497
• /
• 2016

Background Hypertrophic scarring is a pathological condition that occurs after trauma or surgery. Angiogenesis occurs more often with hypertrophic scarring than with normotrophic scarring. The regulation of angiogenesis is one of the key factors in hypertrophic scar management. Vascular endothelial growth factor (VEGF) is an essential factor in the angiogenetic response. This study investigated whether decreasing the level of VEGF is effective for treating hypertrophic scarring. Methods Ten 8-week-old female New Zealand white rabbits were included. Four defects were created on each ear by using a 6-mm punch. Bevacizumab (Avastin, Roche Pharma, Basel, Switzerland) was administered in one ear and normal saline was administered in the other ear. Treatment was administered starting on day 2, every 2 days, until day 14. The levels of VEGF were measured using enzyme-linked immunosorbent assay on day 10 and histologic results were analyzed on day 40. Results Bevacizumab induced-defects showed less hypertrophic scarring when compared with the control group as measured by the scar elevation index (SEI) and loose collagen arrangement. The SEI in the experimental group was $1.89{\pm}0.13$, compared to $1.99{\pm}0.13$ in the control group (n=30, P=0.005). Additionally, the VEGF level was lower ($38.72{\pm}11.03pg$ vs. $82.50{\pm}21.64pg$, n=10, P=0.001) and fewer vessels existed ($8.58{\pm}0.76$ vs. $7.2{\pm}1.20$, n=10, P=0.007). Conclusions Preventing excessive angiogenesis is effective for preventing scar formation, especially with hypertrophic scarring. Although it is not an approach that is sufficient alone for the management of scarring, it may be one of several important strategies for scar treatment.

• Asian Pacific Journal of Cancer Prevention
• /
• v.15 no.1
• /
• pp.175-178
• /
• 2014

Background: Resection rates of lung cancer are low in general and especially in countries like Nepal. Advanced stage at presentation and poor general condition of the patient are the usual causes. Materials and Methods: In this prospective observational study, one hundred cases of lung cancer who presented at the Thoracic Surgery Unit between October 2011 and October 2012 were included. Results: Those aged in the $6^{th}$ and $7^{th}$ decades together accounted for 72/100 patients. The male to female ratio was 2:1. There was a mean-$29.2{\pm}14.2$ pack yrs smoking history with only five non-smokers. Seventy-six patients presented with locally advanced disease while 21 had metastases. Only three had local disease. The average time between onset of symptoms to first contact with a doctor was $2.3{\pm}5.3$ months (range: 0-35.6 months). Average time between first contact to referral was $50.4{\pm}65.7$ days (range-0-365). Only three patients were resected, one after neo-adjuvant chemotherapy. Advanced disease was the cause of unresectability in 95 cases. One of three patients with local disease had pulmonary functions allowing the warranted resection. $N_2$ disease with $T_{1-3}$ on CT scan was found in 47. Three of these patients underwent mediastinoscopy and all confirmed uninvolved $N_2$. Conclusions: Lung resection rates in our center remain low. Late presentation leading to advanced disease and poor pulmonary reserves preclude resection in most cases. More liberal use of mediastinal staging and better assessment of pulmonary functions may allow us to improve resection rates.

• The Korean Journal of Physiology and Pharmacology
• /
• v.10 no.3
• /
• pp.161-165
• /
• 2006

NO and cyclooxygenase-2 (COX-2) are contributes to vascular inflammation induced by various stimulation. The mechanism, which explains a linkage between NO and COX-2, could be of importance in promoting pathophysiological conditions of vessel. We investigated the effects of NO donors on the COX-l and COX-2 mRNA/protein expression, as well as the nitrite production in culture medium of vascular smooth muscle cell (VSMC). VSMC was primarily cultured from thoracic aorta of rat. In this experiments, COX-l and COX-2 mRNA/protein expressions were analysed and nitrite productions were investigated using Griess reagent. VSMC did not express COX-2 protein in basal condition (Nonlipopolysaccharide (LPS) stimulated). In LPS-stimulated experiments, after 3 hours of NO donor pretreatment, LPS $10{\mu}g/ml$ was treated for 24 hours. COX-l protein expressions were unchanged by SNP and NOR-3. NOR-3 significantly increased COX-2 mRNA/protein expression under LPS stimulation. In contrast, SNP did not increase COX-2 mRNA/protein expression under LPS stimulation. Nitrite production was higher in NOR-3 treatment than SNP treatment under LPS stimulation. These results suggest that the expression of COX-2 in VSMC is regulated by NOR-3, COX-2 expressions were depending on the types of NO donor and LPS stimulation in VSMC.

• The Korean Journal of Physiology and Pharmacology
• /
• v.4 no.5
• /
• pp.385-391
• /
• 2000

Using the patch-clamp technique, we investigated the alteration of 4-aminopyridine(4-AP)-sensitive, voltage-dependent $K^+$ channel (Kv) in the mesenteric arterial smooth muscle cell (MASMC) of renovascular hypertensive model, one-kidney one-clip Goldblatt hypertensive rat (GBH). To isolate $K_V$ current, internal pipette solution contained 5 mM ATP and 10 mM EGTA. Under these condition, MASMC was depolarized by 4-AP, but charybdotoxin did not affect membrane potential. Membrane potential of hypertensive cell $(-40.3{\pm}3.2\;mV)$ was reduced when compared to that of normotensive cell $(-59.5{\pm}2.8\;mV).$ Outward $K^+$ current of hypertensive cell was significantly reduced when compared to normotensive cell. At 60 mV, the outward currents were $19.10{\pm}1.91$ and $14.06{\pm}1.05$ pA/pF in normotensive cell and hypertensive cell respectively. 4-AP-sensitive $K^+$ current was also smaller in hypertensive cell $(4.28{\pm}0.38\;pA/pF)$ than in normotensive cell $(7.65{\pm}0.52\;pA/pF).$ The values of half activation voltage $(V_{1/2})$ and slope factor (k1) as well as the values of half inactivation voltage $(V_{1/2})$ and slope factor (k1) were virtually similar between GBH and NTR. These results suggest that the decrease of 4-AP-sensitive $K^+$ current contributes to a depolarization of membrane potential, which leads to development of vascular tone in GBH.

• Journal of Ginseng Research
• /
• v.28 no.4
• /
• pp.211-214
• /
• 2004

This study was carried out to find out the optimum hardening condition for ginseng plantlets redifferentiated by tissue culture method. While a lot of root hair were observed on the root of seedling grown on the soil, few root hair were observed on the root of plantlet redifferentiated in vitro. On the medium solidified with $0.1{\%}$ phytagel, root hair was not observed and root weight, root width and laternal root development were also very poor. While raising the phytagel concentration on the media, root hair began to increase and root weight, root width and latemal root development were improved. Vascular tissue of plantlet grown on the medium with $0.1{\%}$ phytagel was very poor, but that of plantlet grown on the medium with $0.8{\%}$ phytagel was very good.

• The Journal of Korea Assosiation for Disability and Oral Health
• /
• v.6 no.1
• /
• pp.15-18
• /
• 2010

Sturge-Weber syndrome is a rare nonhereditary developmental condition that is characterized by a hamartomatous vascular proliferation involving the tissue of brain and face. The clinical features are characterized by port wine nevus following one or more divisions of trigeminal nerve, ocular involvement and neurologic involvement such as epilepsy, mental retardation, and contralateral hemiplegia. Oral manifestations include unilateral blood vessel expansion of the oral mucosa, vascular hyperplasia of gingiva, pyogenic granuloma-like massive hemangiomatous proliferation of oral mucosa, macrodontia, ipsilateral macroglossia, blood vessel anomaly of maxilla or mandible and abnormal tooth eruption sequence. This case report is about 11-year-old Sturge-Weber syndrome patient presented port wine nevus on the face, venous malformation on soft plate and buccal mucosa. In this case we performed simple extraction of several deciduous teeth and periodic oral hygiene management. If a patient with Sturge-Weber syndrome has to undergo dental surgery in affected areas of the mouth, great care must be taken to prevent severe hemorrhage.

• The Journal of Internal Korean Medicine
• /
• v.21 no.1
• /
• pp.46-54
• /
• 2000

Objectives : Talmyung-san(TMS) has been used for treatment of brain diseases in Chinese traditional medicine. However, little is known about the mechanism by which TMS rescues brain cells from ischemic damages. To elucidate the protective mechanisms of TMS, we execute experiments. Methods : The effects of TMS on ischemia/reperfusion-induced cytotoxicity and generation of nitric oxide(NO) are investigated in primary neonatal myocardial cells and A7rS, aortic smooth muscle cell line. Results : Ischemia/reperfusion itself induces severe myocardial cell death in vitro. However, treatment of the cells with TMS significantly reduces both ischemia/reperfusion-induced myocardial cell death and LDH release. In addition, pretreatment of TMS before reperfusion recovers the lose of beating rates alter ischemia/reperfusion. For a while, the water extract of TMS stimulates myocardial cells to produce NO in a dose dependent manner and it protects the damage of ischemia/reperfusion-induced myocardial cells. Furthermore, the protective effects of the water extract of TMS is mimicked by treatment of sodium nitroprusside, an exogenous NO donor. NG-monomethyl-L-arginine (NGMMA), a specific inhibitor of nitric oxide synthase(NOS), significantly blocks the protective effects of TMS on the cells after ischemia/reperfusion. In addition, on ischemia the water extract of TMS induce NO in A7r5 cell. Conclusions : Taken together, we suggest that the protective effects of TMS against ischemia/reperfusion-induced myocardial damages may be mediated by NO production of myocardial and vascular smooth muscle cell during ischemic condition.

• Investigative Magnetic Resonance Imaging
• /
• v.18 no.3
• /
• pp.253-257
• /
• 2014

Wandering spleen is a rare clinical condition caused by lax splenic suspensory ligaments. The laxity of ligaments causes torsion of splenic vascular pedicle. CT scan of a 7-year-old girl with abdominal pain showed a non-enhancing lobular mass in lower abdomen. Small bowel loops were located at the right-sided abdomen and colonic loops at the left-sided abdomen. MRI scan showed non-enhancing heterogeneous mass with twisted vascular pedicle. To our knowledge, only a few cases have been reported about wandering spleen diagnosed on MRI.