Posttraumatic incarceration of medial collateral ligament into knee joint with anterior cruciate ligament injury

Medial collateral ligament of the knee is an important coronal stabiliser and often injured in isolation or as combination of injuries. The article reports a case of incarcerated medial collateral ligament (MCL) injury in combination with anterior cruciate ligament (ACL) injury in 20 year old male who presented to us 4 weeks after injury. Clinical examination and MRI was correlated to complete ACL tear with torn distal MCL and incarceration into the joint. Patient was taken up for ACL hamstring graft reconstruction with mini-arthrotomy and repair of the torn MCL. Patient was followed up with dedicated rehabilitation protocol with good functional results. At one year follow-up, patient exhibited full range of motion with negative Lachman, Pivot shift and valgus stress tests. This article highlights the rare pattern of MCL tear and also reviews the literature on this pattern of injury.     

Malignant pheochromocytoma: current status and initiatives for future progress

Pheochromocytomas are rare catecholamine-producing neuroendocrine tumors that are usually benign, but which may also present as or develop into a malignancy. Predicting such behavior is notoriously difficult and there are currently no curative treatments for malignant tumors. This report follows from a workshop at the Banbury Conference Center, Cold Spring Harbor, New York, on the 16th-18th November 2003, held to review the state of science and to facilitate future progress in the diagnosis and treatment of malignant pheochromocytoma. The rarity of the tumor and the resulting fragmented nature of studies, typically involving small numbers of patients, represent limiting factors to the development of effective treatments and diagnostic or prognostic markers for malignant disease. Such development is being facilitated by the availability of new genomics-based tools, but for such approaches to succeed ultimately requires comprehensive clinical studies involving large numbers of patients, stringently collected clinical data and tumor samples, and interdisciplinary collaborations among multiple specialist centers. Nevertheless, the well-characterized hereditary basis and the unique functional nature of these neuroendocrine tumors provide a useful framework that offers advantages for establishing the pathways of tumorigenesis and malignancy. Such findings may have relevance for understanding the basis of other more common malignancies where similar frameworks are not available. As the relevant pathways leading to pheochromocytoma are established it should be possible to take advantage of the new generation of drugs being developed to target specific pathways in other malignancies. Again the success of this will require well-designed and coordinated multi-center studies.     

Release of cardiac troponin I after temporally graded acute coronary ischaemia with electrocardiographic ST depression

BACKGROUND: Elevation of cardiac biochemical markers and ST segment depression in the electrocardiogram have important roles in the risk stratification of unstable coronary syndromes. We assessed graded duration of acute coronary ischaemia with ST depression versus release of cardiac troponin I (cTnI) and conventional cardiac markers in 15 ischaemic pigs and 11 controls. METHODS: Coronary ischaemia was induced via percutaneous technique by semiinflating an angioplasty balloon in the left circumflex artery. Blood velocity monitored by Doppler was reduced until ST depression > or =0.1 mV was obtained. Among 26 pigs, six controls had jugular vein sheath introduced only, five controls jugular vein and bilateral femoral sheaths, and 15 pigs were divided into three equal groups (n=5) in which ischaemia was maintained for 10, 20 and 30 min, respectively. RESULTS: Mean blood flow velocity (cm/s) at baseline was 16.3+/-6.5 and was reduced to 4.1+/-3.2 (25% of normal, range 20-29%) during ischaemia. cTnI (microg/l) did not increase in controls but increased from 0.05 to 0.52 (P<0.05) and 0.76 (P<0.05) with 10 and 20 min of ischaemia, and to 30.77 (P<0.05) with 30 min of ischaemia. A rise of myoglobin and conventional cardiac enzymes did not distinguish controls with arterial cut-down from the ischaemia groups. CONCLUSION: Release of cTnI depends on the duration of ST depression ischaemia. The critical time for a major release seems to be between 20 and 30 min. Thus, very early intervention in patients with prolonged ST depression ischemia should be focused on in future clinical trials.     

Investigation of the Mechanical Properties of Mn-Alloyed Tin-Silver-Copper Solder Solidified with Different Cooling Rates

Manganese can be an optimal alloying addition in lead-free SAC (SnAgCu) solder alloys because of its low price and harmless nature. In this research, the mechanical properties of the novel SAC0307 (Sn/Ag0.3/Cu0.7) alloyed with 0.7 wt.% Mn (designated as SAC0307-Mn07) and those of the traditionally used SAC305 (Sn96.5/Ag3/Cu0.5) solder alloys were investigated by analyzing the shear force and Vickers hardness of reflowed solder balls. During the preparation of the reflowed solder balls, different cooling rates were used in the range from 2.7 K/s to 14.7 K/s. After measuring the shear force and the Vickers hardness, the structures of the fracture surfaces and the intermetallic layer were investigated by SEM (Scanning Electron Microscopy). The mechanical property measurements showed lower shear force for the SAC0307-Mn07 alloy (20–25 N) compared with the SAC305 alloy (27–35 N), independent of the cooling rate. However, the SAC0307-Mn07 alloy was softer; its Vickers hardness was between 12 and 13 HV, whereas the Vickers hardness of the SAC305 alloy was between 19 and 20 HV. In addition, structural analyses revealed rougher intermetallic compound layers in the case of the SAC0307-Mn07 alloy, which can inhibit the propagation of cracks at the solder–substrate interface. These two properties of SAC0307-Mn07 alloy, the softer nature and the rougher intermetallic layer, might result in better thermomechanical behavior of the solder joints during the lifetime of electronic devices.     

CD4/CD8 ratio is a promising candidate for non-invasive measurement of liver fibrosis in chronic HCV-monoinfected patients

The extent of liver fibrosis is an important factor in prognosis and clinical decision-making in chronic hepatitis C virus (HCV) infection. We investigated CD4/CD8 ratio in HCV-monoinfected and HIV/HCV-coinfected patients, in order to reveal its relation with liver fibrosis. CD4/CD8 ratio in the peripheral blood was assessed by flow cytometry in a cohort of 19 HCV-monoinfected, 14 HIV/HCV-coinfected, ten HIV-monoinfected patients and 15 healthy controls. Liver fibrosis was assessed by transient elastography (n?=?25) or by liver biopsy (n?=?8). Coinfection with HIV was associated with decreased CD4/CD8 ratios in chronic HCV-infected patients, despite adequate antiretroviral treatment. Furthermore, HCV-monoinfected patients with F3-F4 liver fibrosis demonstrated much lower CD4/CD8 ratios than patients with F0-F2 fibrosis (1.4 versus 2.5, p?=?0.023). Similarly, we observed a strong negative correlation between the CD4/CD8 ratio and liver stiffness measured by transient elastography (R?=??0.78, p?=?0.0006). ROC analysis revealed that CD4/CD8 ratio as a non-invasive marker for fibrosis is very promising (area under the curve 0.8). Although our study was performed with a relatively small number of patients, our findings suggest that the CD4/CD8 ratio is a promising candidate for non-invasive evaluation of liver fibrosis in HCV-monoinfected patients.     

Cinnamaldehyde inhibits L-type calcium channels in mouse ventricular cardiomyocytes and vascular smooth muscle cells

Cinnamaldehyde (CA), a major component of cinnamon, is known to have important actions in the cardiovascular system, including vasorelaxation and decrease in blood pressure. Although CA-induced activation of the chemosensory cation channel TRPA1 seems to be involved in these phenomena, it has been shown that genetic ablation of Trpa1 is insufficient to abolish CA effects. Here, we confirm that CA relaxes rat aortic rings and report that it has negative inotropic and chronotropic effects on isolated mouse hearts. Considering the major role of L-type Ca²⁺ channels in the control of the vascular tone and cardiac contraction, we used whole-cell patch-clamp to test whether CA affects L-type Ca²⁺ currents in mouse ventricular cardiomyocytes (VCM, with Ca²⁺ as charge carrier) and in mesenteric artery smooth muscle cells (VSMC, with Ba²⁺ as charge carrier). We found that CA inhibited L-type currents in both cell types in a concentration-dependent manner, with little voltage-dependent effects. However, CA was more potent in VCM than in VSMC and caused opposite effects on the rate of inactivation. We found these divergences to be at least in part due to the use of different charge carriers. We conclude that CA inhibits L-type Ca²⁺ channels and that this effect may contribute to its vasorelaxing action. Importantly, our results demonstrate that TRPA1 is not a specific target of CA and indicate that the inhibition of voltage-gated Ca²⁺ channels should be taken into account when using CA to probe the pathophysiological roles of TRPA1.