Mass and non-mass breast MRI patterns: a radiologic approach to sick lobe theory.

BACKGROUND: According to sick lobe theory, one or more lobes of the breast are more prone to the development of carcinoma. However, the implications of this theory in breast magnetic resonance imaging (MRI) are unknown. PURPOSE: To evaluate the MRI appearance of mass type (multifocal and multicentric diseases) and non-mass type (non-mass enhancements) sick lobe patterns, together with the histopathology results. MATERIAL AND METHODS: MRI reports of 2015 patients in two tertiary breast imaging centers between June 2012 and June 2018 were retrospectively reviewed for multifocal-multicentric diseases and segmental, linear, and regional enhancements. A total of 113 patients were included. The specimens obtained by thick needle, vacuum, excisional biopsy/lumpectomy or mastectomy after breast MRI scans were pathologically assessed. The pathologic results were categorized as invasive carcinoma, precursor, and benign proliferative lesions according to the 2012 World Health Organization Classification of Tumors. RESULTS: The percentage of underlying benign and precursor invasive lesions was significantly different in patients with mass and non-mass MRI patterns. While the pathology results of mass type patterns were premalignant and malignant in all cases, nearly half of the underlying histologies were benign proliferative subtypes in patients with non-mass type patterns. CONCLUSION: In this study, the mass and non-mass patterns derived from sick lobe theory were related to different risks of malignancy in the pathological examinations.

The effects of Cinnamaldehyde on early brain injury and cerebral vasospasm following experimental subarachnoid hemorrhage in rabbits.

The neuroprotective and vasodilatory effects of cinnamaldehyde have been widely studied and documented. On the basis of these findings, we hypothesized that cinnamaldehyde exhibits therapeutic effects on subarachnoid hemorrhage-induced early brain injury and cerebral vasospasm. Thirty-two adult male New Zealand white rabbits were randomly divided into four groups of eight rabbits: control, subarachnoid hemorrhage, subarachnoid hemorrhage + vehicle, and subarachnoid hemorrhage + cinnamaldehyde. An intraperitoneal dose of 50 mg/kg cinnamaldehyde was administered 5 min following an intracisternal blood injection, followed by three further daily injections at identical doses. The animals were sacrificed 72 h after subarachnoid hemorrhage was induced. The cross-sectional areas and arterial wall thicknesses of the basilar artery were measured and hippocampal degeneration scores were evaluated. Treatment with cinnamaldehyde was effective in providing neuroprotection and attenuating cerebral vasospasm after subarachnoid hemorrhage in rabbits. It effectively increased the cross-sectional areas of the basilar artery and reduced the arterial wall thickness; in addition, hippocampal degeneration scores were lower in the cinnamaldehyde group. The findings of this study showed, for the first time to our knowledge, that cinnamaldehyde exhibits neuroprotective activity against subarachnoid hemorrhage-induced early brain injury and that it can prevent vasospasm. Potential mechanisms underlying the neuroprotection and vasodilation were discussed. Cinnamaldehyde could play a role in subarachnoid hemorrhage treatment.

Claudin-1 expressions decrease in pterygium with respect to normal conjunctiva.

CONTEXT: Pterygium is the fibrovascular growth of the limbal conjunctiva over cornea. This proliferative nature might have a pathogenesis associated with tight junction proteins. OBJECTIVE: To investigate the tight junction protein claudin-1 expressions in pterygium with respect to normal conjunctiva. MATERIALS AND METHODS: This retrospective study included 28 patients who underwent pterygium surgery with autograft. Claudin-1 expressions were immunohistochemically evaluated in normal and lesional conjunctiva of the same eye. Immunohistochemical evaluation was done with regard of both the intensity and the extent of staining. The distribution of the immunohistochemical scores in pterygium and normal conjunctiva has been compared with using McNemar test. RESULTS: The mean age of the patients was 52.2 ± 11.2 years and male/female ratio was 8/20. Among 28 samples of normal conjunctiva 25 (89.2%) demonstrated a strong immunohistochemical expression with claudin-1 whereas this rate was 10.8% for pterygium samples. Statistical analysis revealed a significant decrease in claudin-1 expressions in pterygium with respect to normal conjunctiva (p < 0.001). DISCUSSION AND CONCLUSIONS: The loss of claudin-1 appears to be involved in the pathogenesis of pterygium and the future studies will elucidate the exact role of tight junction proteins in the invasive and recurrent nature of pterygium.

The effect of flurbiprofen on the development of anencephaly in early stage chicken embryos.

OBJECTIVE: The study investigated the effect of flurbiprofen on the development of anencephaly in early stage chicken embryos. MATERIAL AND METHODS: We looked at four groups with a total of 36 embryos. There was a control group, a normal saline group, a normal-dose group and a high-dose group with ten, ten, eight and eight eggs with embryo respectively. RESULTS: Two embryos in the control group, studied with light microscopy at 48 h, were consistent with 28-29 hours' incubation in the Hamburger-Hamilton System. They had open neural tubes. The other embryos in this group were considered normal. One embryo in the normal saline group was on the occlusion stage at 48 h. One embryo showed an open neural tube. They were compatible with 28-29 hours' incubation in the Hamburger-Hamilton system. The remaining eight embryos showed normal development. In the normal dose group, one embryo showed underdevelopment of the embryonic disc and the embryo was dead. In four embryos, the neural tubes were open. One cranial malformation was found that was complicated with anencephaly in one embryo. In two embryos the neural tubes were closed, as they showed normal development, and they reached their expected stages according to the Hamburger-Hamilton classification. There was no malformation or growth retardation. Four experimental embryos were anencephalic in the high dose group, and three embryos had open neural tubes. One embryo exhibited both anencephaly and a neural tube closure defect. None of the embryos in this group showed normal development. CONCLUSIONS: Even the usual therapeutic doses of flurbiprofen increased the risk of neural tube defect. Flurbiprofen was found to significantly increase the risk of anencephaly. The provision of improved technical materials and studies with larger sample sizes will reveal the stage of morphological disruption during the development of embryos.

Attenuation of cerebral vasospasm and secondary injury by testosterone following experimental subarachnoid hemorrhage in rabbit.

BACKGROUND: The vasodilatator effects of testosterone have been widely studied and demonstrated. Based on previous studies of these vasodilatatory activities, we hypothesized that testosterone might have potential effects on subarachnoid hemorrhage-induced cerebral vasospasm. METHODS: Thirty-two adult male New Zealand white rabbits were randomly divided into four groups of eight rabbits in each group: group 1 (control); group 2 (subarachnoid hemorrhage); group 3 (subarachnoid hemorrhage + vehicle); and group 4 (subarachnoid hemorrhage + testosterone). Testosterone (15 mg/kg, intraperitoneally) was administered 5 min after the intracisternal blood injection and continued for 72 h once per day in the same dose for group 4. Animals were killed 72 h after subarachnoid hemorrhage. Basilar artery cross-sectional areas, arterial wall thicknesses, and hippocampal degeneration scores were evaluated in all groups. RESULTS: Intraperitoneal administration of testosterone was found to attenuate cerebral vasospasm and provide neuroprotection after subarachnoid hemorrhage in rabbits. Testosterone treatment was determined to be effective at increasing the luminal area and reducing the wall thickness of the basilar artery. CONCLUSIONS: Our findings show that testosterone has some preventive effects on SAH-induced vasospasm and secondary neuronal injury in rabbits. We propose that the vasodilatatory activity of testosterone is due to its effects on inhibiting calcium channels, activating potassium channels, augmenting nitric oxide synthesis, and inhibiting oxidant stress and inflammation.

The comparative effects of recombinant human erythropoietin and darbepoetin-alpha on cerebral vasospasm following experimental subarachnoid hemorrhage in the rabbit.

BACKGROUND: Darbepoetin alpha is a hypersialylated analogue of erythropoietin effective for activating erythropoietin-receptors. This study investigated the vasodilator and neuroprotective effects of darbepoetin alpha on an experimental subarachnoid hemorrhage model and compared it with erythropoietin. METHODS: Forty adult male New Zealand white rabbits were randomly divided into four groups of ten rabbits each: group 1 (control), group 2 (subarachnoid hemorrhage), group 3 (erythropoietin), and group 4 (darbepoetin alpha). Recombinant human erythropoietin was administered at a dose of 1,000 U/kg intraperitoneally after the induction of subarachnoid hemorrhage and continued every 8 h up to 72 h. Darbepoetin alpha was administered at a single intraperitoneal dose of 30 µg/kg. Animals were killed 72 h after subarachnoid hemorrhage. Basilar artery cross-sectional areas, arterial wall thicknesses, hippocampal degeneration scores and biochemical analyses were measured in all groups. RESULTS: Both erythropoietin and darbepoetin alpha treatments were found to attenuate cerebral vasospasm and provide neuroprotection after subarachnoid hemorrhage in rabbits. Darbepoetin alpha revealed better morphometric and histopathological results than erythropoietin among experimental subarachnoid hemorrhage-induced vasospasm. CONCLUSIONS: Our findings, for the first time, showed that darbepoetin alpha can prevent vasospasm and provides neuroprotection following experimental subarachnoid hemorrhage. Moreover, darbepoetin alpha showed better results when compared with erythropoietin.

Neuroprotective Effects of Coenzyme Q10 and Ozone Therapy on Experimental Traumatic Spinal Cord Injuries in Rats.

OBJECTIVE: This study investigates the neuroprotective effects and functional recovery potential of Coenzyme Q10 (CoQ10) and ozone therapy in spinal cord injury (SCI). MATERIAL AND METHODS: In this study, 40 female Sprague-Dawley rats were divided into 5 groups of 8. Surgical procedures induced spinal cord trauma in all groups, except the control group. The ozone group received 0.7 mg/kg rectal ozone daily for 7 days, starting 1 hour postspinal cord trauma. The CoQ10 group was administered 120 mg/kg CoQ10 orally once daily for 7 days, beginning 24 hours prior to trauma. The CoQ10 + ozone group received both treatments. Examinations included a modified Tarlov scale and inclined plane test on days 1, 3, 5, and 7. Malondialdehyde (MDA) analysis was conducted on serum samples, and assessments of caspase-3, Bcl-2, and Bax levels were performed on tissue samples. Additionally, a comprehensive examination analyzed histopathological and ultrastructural changes. RESULTS: After SCI, there was a statistically significant increase in serum MDA, tissue caspase-3, and Bax levels (MDA P < 0.001, caspase-3 P < 0.001, Bax P = 0.003). In the CoQ10 + ozone group, serum MDA (P = 0.002), tissue caspase-3 (P = 0.001), and Bax (P = 0.030) levels were significantly lower compared to the trauma group. Tissue Bcl-2 levels were also significantly higher (P = 0.019). The combined treatment group demonstrated improved histopathological, ultrastructural, and neurological outcomes. CONCLUSIONS: This study shows that CoQ10 + ozone therapy in traumatic SCI demonstrates neuroprotective effects via antioxidant and antiapoptotic mechanisms. The positive effects on functional recovery are supported by data from biochemical, histopathological, ultrastructural, and neurological examinations.

Antioxidant and antigenotoxic effects of lycopene in obstructive jaundice.

BACKGROUND: Obstructive jaundice, a frequently observed condition caused by obstruction of the common bile duct or its flow and seen in many clinical situations, may end up with serious complications like sepsis, immune depression, coagulopathy, wound breakdown, gastrointestinal hemorrhage, and hepatic and renal failures. Intrahepatic accumulation of reactive oxygen species is thought to be an important cause for the possible mechanisms of the pathogenesis of cholestatic tissue injury from jaundice. Carotenoids have been well described that are able to scavenge reactive oxygen species. Lycopene, a carotenoid present in tomatoes, tomato products, and several fruits and vegetables, have been suggested to have antioxidant activity, so may play a role in certain diseases related to the oxidative stress. The aim of the present study was to determine the effects of lycopene on oxidative stress and DNA damage induced by experimental biliary obstruction in Wistar albino rats. MATERIALS AND METHODS: Daily doses of 100 mg/kg lycopene were given to the bile duct-ligation (BDL) rats orally for 14 days. DNA damage was evaluated by an alkaline comet assay. The levels of aspartate transferase, amino alanine transferase, gamma glutamyl transferase, alkaline phosphatase, and direct bilirubin were analyzed in plasma for the determination of liver functions. The levels of malondialdehyde, reduced glutathione, nitric oxide, catalase, superoxide dismutase, and glutathione S transferase were determined in the liver and kidney tissues. Pro-inflammatory cytokine tumor necrosis factor-alpha level was determined in the liver tissues. Histologic examinations of the liver and kidney tissues were also performed. RESULTS: According to this study, lycopene significantly recovered the parameters of liver functions in plasma, reduced malondialdehyde and nitric oxide levels, enhanced reduced glutathione levels, as well as enhancing all antioxidant enzyme activity in all tissues obtained from the BDL group. Moreover, the parameters of DNA damage in the liver and kidney tissue cells, whole blood cells, and lymphocytes were significantly lower in the lycopene-treated BDL group, compared with the BDL group. CONCLUSIONS: Lycopene significantly reduced the DNA damage, and markedly recovered the liver and kidney tissue injuries seen in rats with obstructive jaundice.

The protective effect of 2-mercaptoethane sulfonate (MESNA) against traumatic brain injury in rats.

BACKGROUND: The agent, 2-mercaptoethane sulfonate (MESNA), is a synthetic small molecule, widely used as a systemic protective agent against chemotherapy toxicity, but is primarily used to reduce hemorrhagic cystitis induced by cyclophosphamide. Because MESNA has potential antioxidant and cytoprotective effects, so we hypothesized that MESNA may protect the brain against traumatic injury. METHOD: Thirty-two rats were randomized into four groups of eight animals each; Group 1 (sham), Group 2 (trauma), Group 3 (150 mg/kg MESNA), Group 4 (30 mg/kg methylprednisolone). Only skin incision was performed in the sham group. In all the other groups, the traumatic brain injury model was created by an object weighing 450 g falling freely from a height of 70 cm through a copper tube on to the metal disc over the skull. The drugs were administered immediately after the injury. The animals were killed 24 h later. Brain tissues were extracted for analysis, where levels of tissue malondialdehyde, caspase-3, glutathione peroxidase, superoxide dismutase, nitric oxide, nitric oxide synthetase and xanthine oxidase were analyzed. Also, histopathological evaluation of the tissues was performed. RESULTS: After head trauma, tissue malondialdehyde levels increased; these levels were significantly decreased by MESNA administration. Caspase-3 levels were increased after trauma, but no effect of MESNA was determined in caspase-3 activity. Following trauma, both glutathione peroxidase and superoxide dismutase levels were decreased; MESNA increased the activity of both these antioxidant enzymes. Also, after trauma, nitric oxide, nitric oxide synthetase and xanthine oxidase levels were increased; administration of MESNA significantly decreased the levels of nitric oxide, nitric oxide synthetase and xanthine oxidase, promising an antioxidant activity. Histopathological analysis showed that MESNA protected the brain tissues well from injury. CONCLUSIONS: Although further studies considering different dose regimens and time intervals are required, MESNA was shown to be at least as effective as methylprednisolone in the traumatic brain injury model.

Study the effects of zonisamide on fine structure of rabbit basilar artery and hippocampus in rabbit subarachnoid hemorrhage model.

BACKGROUND: In this study, we investigated the effect of a novel antiepileptic drug, zonisamide (ZNS), on the basilar artery and hippocampus in a rabbit subarachnoid hemorrhage (SAH) model. METHODS: Three groups of New Zealand white rabbits were used: a sham (non-SAH) group, an SAH + saline group, and SAH + drug treatment group that received ZNS. In the treatment group, the subjects were given ZNS for 3 days after the SAH. Hippocampal sections were evaluated for neural tissue degeneration. Basilar artery lumen areas and arterial wall thickness were also measured in all groups. RESULTS: The mean luminal area of the SAH + ZNS was significantly greater than the SAH + saline group. In addition, the arterial wall thickness of SAH + ZNS group was significantly thinner than the SAH + saline group. The neuronal degeneration scores of the hippocampal CA1 regions in the SAH + ZNS group were significantly lower than the SAH + saline treatment animals. CONCLUSIONS: These results indicate that ZNS has a vasodilatatory effect on the basilar artery and a neuronal protective effect in the CA1 region of the hippocampus in a rabbit SAH model.

Neuroprotective Effects of Niacin on Ischemia/Reperfusion Injury of the Rabbit Spinal Cord.

OBJECTIVE: Previous studies have shown niacin has neuroprotective effects on the central nervous system. However, its specific effect on spinal cord ischemia/reperfusion injury has not yet been explored. This study aims to evaluate whether niacin can contribute neuroprotective effects on spinal cord ischemia/reperfusion injury. METHODS: Rabbits were randomized into 4 groups of 8 animals: group I (control), group II (ischemia), group III (30 mg/kg methylprednisolone, intraperitoneal), and group IV (500 mg/kg niacin, intraperitoneal). The rabbits in group IV were premedicated with niacin for 7 days prior to inducing ischemia/reperfusion injury. The control group was subjected only to a laparotomy, while the remaining groups underwent spinal cord ischemia through a 20-minute occlusion of the aorta caudal to the left renal artery. Following the procedure, levels of catalase, malondialdehyde, xanthine oxidase, myeloperoxidase, and caspase-3 were analyzed. Ultrastructural, histopathological, and neurological evaluations were also performed. RESULTS: Spinal cord ischemia/reperfusion injury resulted in increased levels of xanthine oxidase, malondialdehyde, myeloperoxidase, and caspase-3, with a concomitant decrease in catalase levels. Treatment with methylprednisolone and niacin led to decreased levels of xanthine oxidase, malondialdehyde, myeloperoxidase, and caspase-3 and an increase in catalase. Both methylprednisolone and niacin treatments demonstrated improvements in histopathological, ultrastructural, and neurological assessments. CONCLUSIONS: Our findings suggest that niacin has antiapoptotic, anti-inflammatory, antioxidant, and neuroprotective effects at least equal to methylprednisolone in ischemia/reperfusion injury of the spinal cord. This study is the first to report the neuroprotective impact of niacin on spinal cord ischemia/reperfusion injury. Further research is warranted to elucidate the role of niacin in this context.

Cerebrolysin Amelioration of Spinal Cord Ischemia/ Reperfusion Injury in Rabbit Model.

AIM: To investigate the effects of cerebrolysin on inflammation, oxidative stress, apoptosis, and neurologic recovery in the setting of an experimental rabbit model of spinal cord ischemia/reperfusion injury (SCIRI). MATERIAL AND METHODS: Rabbits were randomly divided into five groups: control, ischemia, vehicle, methylprednisolone (30 mg/kg), and cerebrolysin (5 ml/kg) group. The rabbits in the control group underwent only laparotomy; the other groups underwent spinal cord ischemia and reperfusion injury for 20 minutes. Neurologic examination after 24 hours was based on the Modified Tarlov scale. Myeloperoxidase activities, catalase and malondialdehyde levels, and caspase-3 concentrations were determined in serum and tissue samples. Serum xanthine oxidase levels were studied and histopathological and ultrastructural changes were examined. RESULTS: After SCIRI, serum and tissue myeloperoxidase activities, malondialdehyde levels, caspase-3 concentrations, and serum xanthine oxidase activities were increased (p < 0.01?0.001). Catalase levels were significantly diminished (p < 0.001). Cerebrolysin treatment correlated with reduced myeloperoxidase and xanthine oxidase activities, malondialdehyde levels and caspase-3 concentrations; and with increased catalase levels (p < 0.001, for all). The cerebrolysin group showed improved histopathological, ultrastructural, and neurological outcomes. CONCLUSION: For the first time in the literature, the current study reports anti-inflammatory, antioxidant, antiapoptotic, and neuroprotective effects of cerebrolysin in a SCIRI rabbit model.

Mildronate Has Ameliorative Effects on the Experimental Ischemia/Reperfusion Injury Model in the Rabbit Spinal Cord.

BACKGROUND: Mildronate is a useful anti-ischemic agent and has antiinflammatory, antioxidant, and neuroprotective activities. The aim of this study is to investigate the potential neuroprotective effects of mildronate in the experimental rabbit spinal cord ischemia/reperfusion injury (SCIRI) model. METHODS: Rabbits were randomized into 5 groups of 8 animals as groups 1 (control), 2 (ischemia), 3 (vehicle), 4 (30 mg/kg methylprednisolone [MP]), and 5 (100 mg/kg mildronate). The control group underwent only laparotomy. The other groups have the spinal cord ischemia model by a 20-minute aortic occlusion just caudal to the renal artery. The malondialdehyde and catalase levels and caspase-3, myeloperoxidase, and xanthine oxidase activities were investigated. Neurologic, histopathologic, and ultrastructural evaluations were also performed. RESULTS: The serum and tissue myeloperoxidase, malondialdehyde, and caspase-3 values of the ischemia and vehicle groups were statistically significantly higher than those of the MP and mildronate groups (P < 0.001). Serum and tissue catalase values of the ischemia and vehicle groups were statistically significantly lower than those of the control, MP, and mildronate groups (P < 0.001). The histopathologic evaluation showed a statistically significantly lower score in the mildronate and MP groups than in the ischemia and vehicle groups (P < 0.001). The modified Tarlov scores of the ischemia and vehicle groups were statistically significantly lower than those of the control, MP, and mildronate groups (P < 0.001). CONCLUSIONS: This study presented the antiinflammatory, antioxidant, antiapoptotic, and neuroprotective effects of mildronate on SCIRI. Future studies will elucidate its possible use in clinical settings in SCIRI.

The effect of thiocolchicoside on cerebral vasospasm following experimental subarachnoid hemorrhage in the rabbit.

BACKGROUND: This study investigated the effects of thiocolchicoside to prevent cerebral vasospasm in a rabbit model of subarachnoid hemorrhage. METHODS: Twenty-four adult male New Zealand white rabbits were randomly divided into three groups of eight rabbits each: group 1 (control), group 2 (subarachnoid hemorrhage), group 3 (treatment). Thiocolchicoside (4 mg/kg, intraperitoneally) was administered just before intracisternal blood injection and continued for 72 h once a day in the same dose for group 3. Animals were killed 72 h after subarachnoid hemorrhage. Basilar artery cross-sectional areas and arterial wall thicknesses were measured in all groups. RESULTS: Intraperitoneal administration of thiocolchicoside was found to attenuate cerebral vasospasm after subarachnoid hemorrhage in rabbits. Thiocolchicoside treatment was determined to be effective in increasing the luminal area and reducing the wall thickness of the basilar artery. CONCLUSIONS: Our findings, for the first time, showed that TCC can prevent vasospasm induced by SAH. Our results also showed that GABAergic activity may play an important role in cerebral vasospasm etiopathogenesis. In conclusion, the thiocolchicoside treatment might be beneficial in preventing vasospasm after subarachnoid hemorrhage, thus showing potential for clinical application.

Effects of darbepoetin-α in spinal cord ischemia-reperfusion injury in the rabbit.

BACKGROUND: Darbepoetin-alpha (DA) is a novel erythropoiesis-stimulating agent developed for treating anemia. In animal models, recombinant human erythropoietin has been reported to be beneficial for neuroprotection. In this study, we determined whether DA would protect the spinal cord against ischemia-reperfusion injury in a rabbit model. METHODS: Forty rabbits were randomized into five groups of eight animals each: group 1 (sham), group 2 (ischemia), group 3 (vehicle), group 4 (30 mg/kg methylprednisolone), group 5 (30 µg/kg DA). Only laparotomy was performed in the sham group. In all the other groups, the spinal cord ischemia model was created by a 20-min occlusion of the aorta just caudal to renal artery with an aneurysm clip. The drugs were administered immediately after the clamp was removed. The animals were killed 24 h later. Spinal cord segments between L2 and L5 were harvested for analysis. Neurological evaluation was performed with the Tarlov scoring system just before the animals were killed. Level of tissue malondialdehyde was analyzed as a marker of lipid peroxidation and tissue caspase-3 activity as a marker of apoptosis. Also, histopathological evaluation of the tissues was performed. RESULTS: Both malondialdehyde and caspase-3 levels were significantly decreased by DA administration. Histopathological evaluation of the tissues also demonstrated decrease in neuronal degeneration and infiltration parameters after DA administration. In the DA group, neurological outcome scores were statistically significantly better compared with the ischemia and the vehicle groups. CONCLUSIONS: Although further studies considering different dose regimens and time intervals are required, DA was shown to be at least as effective as methylprednisolone in spinal cord ischemia/reperfusion model.

Primary necrotizing fasciitis of the breast. Case series with 5 patients.

Necrotizing fasciitis (NF) is an aggressive, necrotic, life-threatening infection of the soft tissues. The delay on treatment is generally accompanied by almost 90 % lethality according to the development of septic shock and its associated complications. Primary Necrotizing Fasciitis of the Breast (PNFB) is seen extremely rare. To date, breast necrotizing fasciitis have been reported only as a limited number of case reports in the literature. PNFB is commonly misdiagnosed as cellulitis, mastitis, abscess or inflammatory breast cancer. Although PNFB is a very rapid and aggressive disease, which can be fatal. Delayed cases were unfortunately resulted in mortality due to several consequential reasons. Therefore, careful and detailed evaluation of all cases irrespective of age, especially those with risk factors and comorbidities, could be life saving in respect of early diagnosis and timely treatment. Our aim is to to present the analysis and treatment modalities of five primarily seen PFNB, in this case series.

Quantitative perfusion parameters of benign inflammatory breast pathologies: A descriptive study.

PURPOSE: With this study, we evaluated the perfusion magnetic resonance imaging (MRI) features of benign inflammatory breast lesions for the first time and compared their Ktrans, Kep, Ve values and contrast kinetic curves to benign masses and invasive ductal carcinoma (IDC). MATERIALS AND METHODS: Perfusion MRIs of the benign masses (n = 42), inflammatory lesions (n = 25), and IDCs (n = 16) were evaluated retrospectively in terms of Ktrans, Kep, Ve values and contrast kinetic curves and compared by the Kruskal-Wallis, Mann-Whitney U, chi-square tests statistically. Cronbach α test was used to measure intraobserver and interobserver reliability. RESULTS: Mean Ktrans values were 0.052 for benign masses, 0.086 for inflammatory lesions and 0.101 for IDC (p < 0.001). Mean Kep values were 0.241 for benign masses, 0.435 for inflammatory lesions and 0.530 for IDC (p < 0.001). Mean Ve values were 0.476 for benign masses, 0.318 for inflammatory lesions and 0.310 for IDC (p = 0.067). For inflammatory and IDC lesions, Ktrans and Kep values were found to be higher and Ve values were lower than benign masses (p = 0.001 for Ktrans, p = 0.001 for Kep, p = 0.045 for Ve). There were excellent or good intra-interobserver reliabilities. For the kinetic curve pattern, most of the benign lesions showed progressive (81%), inflammatory lesions progressive (64%) and IDC lesions plateau (75%) patterns (p < 0.001). CONCLUSIONS: On T1 perfusion MRI, similar to IDC lesions, inflammatory lesions demonstrate higher Ktrans and Kep and lower Ve values than benign masses. Quantitative perfusion parameters are not helpful in differentiating them from IDC lesions.

Amelioration of Cerebral Vasospasm and Secondary Injury by Vigabatrin After Experimental Subarachnoid Hemorrhage in the Rabbit.

BACKGROUND: Vigabatrin, an antiepileptic drug, increases the level of gamma aminobutyric acid in the brain by inhibiting its catabolism. Because gamma aminobutyric acid has been proved to have vasodilatory effects, in the present study, we investigated the effect of vigabatrin to treat experimental subarachnoid hemorrhage (SAH)-induced vasospasm. METHODS: A total of 30 New Zealand white rabbits were divided into 3 groups of 10 each: the control group, SAH group, and vigabatrin group. Experimental SAH was established by injection of autologous arterial blood into the cisterna magna. In the vigabatrin group, the rabbits were administered vigabatrin for 3 days after induction of the SAH. The first dose of vigabatrin was given 2 hours after SAH induction. A daily dose of 500 mg/kg vigabatrin was administered intraperitoneally. After 3 days, the rabbits were sacrificed, and the brains were removed, together with the cerebellum and brainstem. The basilar artery wall thickness and lumen areas were measured. The neuronal degeneration in the hippocampus (CA1, CA3, and dentate gyrus) was also evaluated. RESULTS: The arterial wall thickness of the vigabatrin group was less than that in the SAH group (P < 0.001), and the mean luminal area of the vigabatrin group was greater than that in the SAH group (P < 0.001). Additionally, the hippocampal neuronal degeneration score of the vigabatrin group was lower than that of the SAH group (P < 0.001). CONCLUSION: These findings have indicated that vigabatrin has a vasodilatory effect in an experimental SAH model in the rabbit. Moreover, it showed a neuroprotective effect in the hippocampal neurons against secondary injury induced by SAH.

The Vasorelaxant and Neuroprotective Effects of Mildronate in A Rabbit Subarachnoid Hemorrhage Model.

AIM: To investigate the effects of an anti-ischemic agent, mildronate, on subarachnoid hemorrhage-induced vasospasm. MATERIAL AND METHODS: Rabbits were randomly divided into four groups: control, subarachnoid hemorrhage (SAH), vehicle, and mildronate (n=8 animals per group). In the treatment group, 200 mg/kg of mildronate were intraperitoneally administered 5 minutes after the procedure and continued for 3 days as daily administrations of the same dose. At the end of the third day, the cerebrum, cerebellum, and brain stem were perfused, fixated, and removed for histopathological examination. Tissues were examined for arterial wall thickness, luminal area, and hippocampal neuronal degeneration. RESULTS: Mildronate group showed significantly increased luminal area and reduced wall thickness of the basilar artery compared with the subarachnoid hemorrhage group. In addition, the hippocampal cell degeneration score was significantly lower in the mildronate group than in the SAH and vehicle groups. CONCLUSION: These results show that mildronate exerts protective effects against SAH-induced vasospasm and secondary neural injury.

Tissue oxidative stress level and remote organ injury in two-hit trauma model of sequential burn injury and peritoneal sepsis are attenuated with N-acetylcysteine treatment in rats.

BACKGROUND: The second hit in trauma leads to an exaggerated inflammatory response and multiple organ failure. Infection following burn injury is a useful model for two-hit trauma studies. The aim of this study was to investigate the effect of N-acetylcysteine (NAC) treatment as an antioxidant in a two-hit trauma model. METHODS: 30% scalding burn injury was performed in 45 rats and cecal ligation-puncture (CLP) was performed 72 hours later. Groups were allocated as follows: Group I: No treatment was performed; Group II: Rats were treated with 150 mg/kg/day i.p. NAC for 72 h following CLP; Group III: Rats were treated with 150 mg/kg/day i.p. NAC for 6 days following thermal injury. Tissue samples were collected to study the tissue malonyldialdehyde (MDA) and glutathione (GSH) levels, and for histopathological examination on day 7. RESULTS: No difference in mortality between groups was detected. Tissue MDA levels significantly decreased in the liver (p=0.01, p=0.02) and ileum (p=0.01, p=0.02) in the treatment groups. Lung tissue GSH levels were found to be significantly increased in Group II (p=0.02). Lung injury scores were decreased in Group II (p=0.005) compared to the control group. CONCLUSION: NAC attenuated tissue oxidative stress level and remote organ injury in two-hit trauma. Further experimental and clinical studies on this subject are necessary.