Parathyroid allotransplantation to treat post-thyroidectomy hypoparathyroidism: A review of case studies.

OBJECTIVE: Symptomatic long-term hypoparathyroidism following thyroid surgery requires an alternative and permanent therapy that would effectively restore parathyroid function and eliminate the need for substitution drug therapy. The aim of this study was to systematically review the literature on the efficacy and safety of parathyroid allotransplantation to treat post-operative hypoparathyroidism. METHODS: MEDLINE, Embase, BIOSIS and the Cochrane Library were searched for published articles (from inception of each database to September 30, 2018). A total of 9 studies comprising 146 patients (177 allotransplantations) with post thyroidectomy hypoparathyroidism were identified. RESULTS: Parathyroid tissues used for allotransplant were cultured parathyroid cells, cryopreserved parathyroid cells and encapsulated microspheres. Post-transplant immunosuppression was only reported in three studies, mainly with oral prednisolone for 2 weeks to 6 months. Mean graft survival following allotransplantation was 47% (95% CI 24%-71%) when patients were followed-up to 6 months and 41% (95% CI 2.3%-80%) at 12 months. There was significant unexplained heterogeneity observed between studies in both these groups (I2 > 50%). Parathyroid hormone (PTH) levels, and serum calcium levels post intervention was not reported in all studies, but available evidence suggests the levels remains higher (PTH level around 12 pg/ml; Ca level around 8 mg/dl) post-allotransplantation for up to 24 months. CONCLUSIONS: Long-term benefit and harms of allotransplantation is still unclear due to the clinical and statistical heterogeneity observed among the studies. Therefore, conduct of a well-designed controlled clinical trial in the immediate future on allotransplantation is of paramount importance.

Kinesin superfamily: roles in breast cancer, patient prognosis and therapeutics.

Breast cancer pathobiology is known to be influenced by the differential expression of a group of proteins called the kinesin superfamily (KIFs), which is instrumental in the intracellular transport of chromosomes along microtubules during mitosis. During cellular division, kinesins are strictly regulated through temporal synthesis so that they are present only when needed. However, their misregulation may contribute to uncontrolled cell growth owing to premature sister chromatid separation, highlighting their importance in cancer. This review covers the functions of kinesins in normal and breast cancer cells, the use of kinesins for breast cancer patient prognosis, and the targeting of these molecules for therapeutics. A better understanding of KIF proteins may be pivotal to improved disease outcomes for breast cancer patients.

SLICC/ACR damage index independently associated with left ventricular diastolic dysfunction in patients with systemic lupus erythematosus.

Left ventricular (LV) diastolic dysfunction has been reported in both active and inactive systemic lupus erythematosus (SLE) patients without clinical evidence of cardiovascular disease. However, the relationship between the long-term inflammatory burden reflected by the SLICC/ACR damage index and LV diastolic function has not been studied. Eighty-two SLE patients and 82 controls matched for age, sex, body mass index, blood pressure and heart rate underwent echocardiography with tissue Doppler imaging (TDI). LV diastolic function was estimated by the myocardial early diastolic velocity (E') at the lateral annulus. There were 51 patients (62.2%) with nephritis, 23 patients (28.0%) with hypertension, 21 patients (25.6%) with vasculitis, 16 patients (19.5%) with pulmonary hypertension, 4 patients (4.9%) with cerebrovascular disease and 2 patients (2.4%) with diabetes mellitus. Sixty-two patients (75.6%) were taking prednisone and 35 patients (42.7%) used a immunosuppressant. Forty-five patients (54.8%) had active disease and suffered from disease-related end-organ damage. Patients with SLICC/ACR damage index ≥1 had more evidence of LV diastolic dysfunction with lower lateral annulus E' (9.6 ± 3.4 vs 12.9 ± 3.5 cm/s, p < 0.001) than those without. In addition, the proportion of patients with abnormal LV myocardial relaxation (defined as lateral E' < 10.0 cm/s) (51.1% vs 16.2%, χ(2) = 10.8, p = 0.001) were significantly higher. Multivariate analysis showed that the SLICC/ACR damage index ≥1 was independently associated with LV diastolic dysfunction (OR = 3.80, 95%CI: 1.21-11.95, p = 0.023) after adjusting for hypertension, disease duration and medical therapy. This may suggest that the overall inflammatory burden in SLE, as reflected by SLICC/ACR damage index, is associated with the development of diastolic dysfunction in SLE patients.

Effects of rosuvastatin on subclinical atherosclerosis and arterial stiffness in rheumatoid arthritis: a randomized controlled pilot trial.

OBJECTIVE: To ascertain the effect of rosuvastatin on carotid atherosclerosis and arterial stiffness in patients with rheumatoid arthritis (RA). METHODS: Fifty RA patients were randomized in a double-blind placebo-controlled trial to receive 10 mg rosuvastatin (n = 24) or placebo (n = 26). Patients were followed prospectively every 3 months for 12 months. Intima-media thickness (IMT), augmentation index (AIx), and subendocardial viability ratio (SEVR) were measured at baseline, 6 and 12 months. RESULTS: Rosuvastatin resulted in statistically significant reductions of total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), apolipoprotein B (Apo B), and urate levels vs. placebo. However, rosuvastatin had no significant effect on changes in inflammatory markers, including C-reactive protein (CRP) levels [from 2.9 (1.4-11.0) to 3.1 (0.9-13.3) mg/L in the rosuvastatin group compared with from 5.8 (2.6-14.2) to 4.4 (1.2-12.3) mg/L in the placebo group]. Nonetheless, a significant improvement in the Disease Activity Score (DAS) and a reduction in fibrinogen level was observed at 6 and 12 months compared with baseline in the rosuvastatin group. The treatment group exhibited a significant increase in SEVR (from 157 ± 28% to 163 ± 33% in the rosuvastatin group compared with from 143 ± 18% to 143 ± 26% in the placebo group, p = 0.023), but no significant effect was observed in the changes in IMT and AIx. CONCLUSION: Our data suggest that rosuvastatin has a modest anti-inflammatory effect in RA patients with low disease activity in terms of reduction in DAS and fibrinogen level. Rosuvastastin may also improve subendocardial perfusion and lower the urate level.

miR-145-dependent targeting of junctional adhesion molecule A and modulation of fascin expression are associated with reduced breast cancer cell motility and invasiveness.

Micro RNAs are small non-coding RNAs, which regulate fundamental cellular and developmental processes at the transcriptional and translational level. In breast cancer, miR-145 expression is downregulated compared with healthy control tissue. As several predicted targets of miR-145 potentially regulate cell motility, we aimed at investigating a potential role for miR-145 in breast cancer cell motility and invasiveness. Assisted by Affymetrix array technology, we demonstrate that overexpression of miR-145 in MDA-MB-231, MCF-7, MDA-MB-468 and SK-BR-3 breast cancer cells and in Ishikawa endometrial carcinoma cells leads to a downregulation of the cell-cell adhesion protein JAM-A and of the actin bundling protein fascin. Moreover, podocalyxin and Serpin E1 mRNA levels were downregulated, and gamma-actin, transgelin and MYL9 were upregulated upon miR-145 overexpression. These miR-145-dependent expression changes drastically decreased cancer cell motility, as revealed by time-lapse video microscopy, scratch wound closure assays and matrigel invasion assays. Immunofluorescence microscopy demonstrated restructuring of the actin cytoskeleton and a change in cell morphology by miR-145 overexpression, resulting in a more cortical actin distribution, and reduced actin stress fiber and filopodia formation. Nuclear rotation was observed in 10% of the pre-miR-145 transfected MDA-MB-231 cells, accompanied by a reduction of perinuclear actin. Luciferase activation assays confirmed direct miR-145-dependent regulation of the 3'UTR of JAM-A, whereas siRNA-mediated knockdown of JAM-A expression resulted in decreased motility and invasiveness of MDA-MB-231 and MCF-7 breast cancer cells. Our data identify JAM-A and fascin as novel targets of miR-145, firmly establishing a role for miR-145 in modulating breast cancer cell motility. Our data provide a rationale for future miR-145-targeted approaches of antimetastatic cancer therapy.

Disease chronicity and activity predict subclinical left ventricular systolic dysfunction in patients with systemic lupus erythematosus.

OBJECTIVE: This study investigates parameters that could predict subclinical cardiac dysfunction in systemic lupus erythematosus (SLE) in the absence of valvular, clinical coronary artery and pericardial disease. DESIGN: A case-control trial. SETTING: Rheumatology clinic, a university teaching hospital. PATIENTS: Eighty-two female SLE patients (49 (SD 9) years) and 82 female normal subjects (49 (13) years) matched for age, body mass index, blood pressure and heart rate. INTERVENTIONS: All underwent standard echocardiography and tissue Doppler imaging. MAIN OUTCOME MEASURES: Twenty-two (27%) patients had evidence of impaired left ventricular (LV) long-axis function with mean myocardial peak systolic velocity (Sm) of basal six segments <4.4 cm/s and also subnormal stress-corrected midwall fractional shortening. Thirty-four (42%) patients demonstrated impaired right ventricular (RV) long-axis function. These occurred in the presence of comparable normal LV ejection fraction, cardiac index, and RV fractional area change to the control group. Patients with subnormal mean Sm were older (49 (8) vs 44 (9); p = 0.043) and had a higher prevalence of hypertension (46% vs 22%; p = 0.034), longer disease duration >10 years (82% vs 50%, p = 0.01), higher disease activity score (73% vs 48% for Systemic Lupus Erythematosus Disease Activity Index (SLEDAI)> or =1, p = 0.049) and end-organ damage index (64% vs 47% with Systemic Lupus International Collaborating Clinics Damage Index (SLICC)> or =1, p = 0.049) than those with normal values. Disease duration >10 years, disease activity index and increased arterial stiffness provided additional incremental predictive value of LV long-axis function. CONCLUSION: SLE patients have subclinical long and short-axis dysfunctions. Regular monitoring of cardiac function by tissue Doppler echocardiography may be indicated for patients who had SLE for >10 years, frequent flare or when arterial stiffening is demonstrated.

Expression of syndecan-2 in the amoeboid microglial cells and its involvement in inflammation in the hypoxic developing brain.

The present study examined the expression of heparan sulphate proteoglycan, syndecan-2 (Sdc-2) in the corpus callosum and the amoeboid microglial cells (AMC) in the neonatal rat brain in response to hypoxia. In 1-day old Wistar rats subjected to hypoxia the mRNA and protein expression of Sdc-2 in the corpus callosum, heavily populated by AMC, was increased up to 3 days after the hypoxic exposure. Immunoexpression of Sdc-2 was localized in AMC as confirmed by double labeling using microglial marker. Primary cultures of microglial cells subjected to hypoxia showed a significant increase in Sdc-2 expression. Application of Sdc-2 to microglial cultures under hypoxia increased the release of tumor necrosis factor-alpha, interleukin-1beta, chemokine (C-C motif) ligand 2 (CCL2), and chemokine (C-X-C motif) ligand 12 (CXCL12) by the microglial cells. Additionally, Sdc-2 enhanced the production of reactive oxygen species (ROS) by microglia subjected to hypoxia. Edaravone [3-methyl-1phenyl-2-pyrazolin-5-one], an antioxidant drug, suppressed the hypoxia- and Sdc-2-induced increased production of cytokines, chemokines, and ROS. In the light of these findings, we suggest that Sdc-2 plays an important role in microglial production of inflammatory cytokines, chemokines, and ROS in hypoxic conditions. In this connection, edaravone suppressed the hypoxia- and Sdc-2-induced increased cytokine and ROS production suggesting its therapeutic potential in ameliorating neuroinflammation.

Hypertension and heart failure: a dysfunction of systole, diastole or both?

The pathological myocardial hypertrophy associated with hypertension contains the seed for further maladaptive development. Increased myocardial oxygen consumption, impaired epicardial coronary perfusion, ventricular fibrosis and remodelling, abnormalities in long-axis function and torsion, cause, to a varying degree, a mixture of systolic and diastolic abnormalities. In addition, chronotropic incompetence and peripheral factors such as lack of vasodilator reserve and reduced arterial compliance further affect cardiac output particularly on exercise. Many of these factors are common to hypertensive heart failure with a normal ejection fraction as well as systolic heart failure. There is increasing evidence that these apparently separate phenotypes are part of a spectrum of heart failure differing only in the degree of ventricular remodelling and volume changes. Furthermore, dichotomizing heart failure into systolic and diastolic clinical entities has led to a paucity of clinical trials of therapies for heart failure with a normal ejection fraction. Therapies aimed at reversing myocardial fibrosis, and targets outside the heart such as enhancing vasodilator reserve and improving chronotropic incompetence deserve further study and may improve the exercise capacity of hypertensive heart failure patients. Hypertension heart disease with heart failure is simply not a dysfunction of systole and diastole. Other peripheral factors including heart rate and vasodilator response with exercise may deserve equal attention in an attempt to develop more effective treatments for this disorder.

Increased arterial stiffness correlated with disease activity in systemic lupus erythematosus.

To evaluate the relationships between arterial stiffness, disease activity and end-organ damage in systemic lupus erythematosus (SLE), non-invasive vascular assessments were made on 32 female SLE patients and 32 female normal controls. The patients had significantly increased brachial-ankle pulse wave velocity (PWV) (13.06 +/- 1.79 vs. 11.50 +/- 1.00 m/s; P < 0.001), heart-ankle PWV (8.98 +/- 1.16 vs. 7.88 +/- 0.73 m/s; P < 0.001), carotid augmentation index (AI) (21.6 +/- 17.2% vs. 5.4 +/- 14.0%; P = 0.001) and carotid intima-medial thickness (IMT) (0.753 +/- 0.132 vs. 0.644 +/- 0.092 mm; P = 0.002) when compared with controls. The disease activity and organ damage were evaluated by SLE disease activity index (SLEDAI) and systemic lupus international collaborating clinics (SLICC) damage index. Patients with active disease (SLEDAI > or = 3) had significantly higher carotid AI (34.4 +/- 9.7% vs. 17.8 +/- 17.3%, P < 0.05) than stable ones (SLEDAI < 3) and those with organ damage (SLICC > or = 1) had significantly higher heart-ankle PWV (9.69 +/- 1.13 vs. 8.61 +/- 1.02 m/s, P < 0.05) than those with SLICC = 0. After making adjustments for age, body mass index (BMI) and blood pressure, carotid AI was found to show correlation with SLEDAI and haPWV with SLICC. A carotid AI value of 33.3% identified SLEDAI > or = 3 with a sensitivity of 83% and a specificity of 80%, whereas a heart-ankle PWV value of 9.0 m/s identified SLICC > or = 1 with a sensitivity of 91% and a specificity of 67%. In conclusion, SLE was an independent risk factor of sub-clinical atherosclerosis and arterial stiffness may identify the presence of active disease.

Improvement of left ventricular myocardial short-axis, but not long-axis function or torsion after cardiac resynchronisation therapy: an assessment by two-dimensional speckle tracking.

AIMS: To evaluate whether short-axis function plays a part in determining left ventricular (LV) geometric and functional improvement after cardiac resynchronisation therapy (CRT). METHODS AND RESULTS: 39 patients who received CRT were enrolled. 2D speckle tracking echocardiography was performed at baseline and three months after CRT to assess mean systolic circumferential (epsilon-circum), radial (epsilon-radial) and longitudinal (epsilon-long) strain and torsion. Responders of reverse remodelling (n = 21) had higher baseline mean epsilon-circum than non-responders (p<0.05), who also had improvement in mean epsilon-circum and mean epsilon-radial (both p<0.05) after CRT. Also, the increase in mean epsilon-circum correlated with increase in ejection fraction (r = 0.57, p<0.001) and decrease in mid-cavity width (r = -0.52, p = 0.001). A baseline mean epsilon-circum of >or=6.5% predicted a gain in ejection fraction >or=5%, with a sensitivity of 73% and a specificity of 71%. The baseline epsilon-long was not different between the two groups, and remained unchanged after CRT. The torsion did not improve in responders, but was worsened in non-responders (p<0.05). CONCLUSIONS: The improvement of LV short-axis function but not long-axis function or torsion contributes to the improvement in LV global function and geometry at three-month follow up. A relatively preserved mean epsilon-circum of >or=6.5% might be useful to predict favourable responses after CRT.

The Hong Kong diastolic heart failure study: a randomised controlled trial of diuretics, irbesartan and ramipril on quality of life, exercise capacity, left ventricular global and regional function in heart failure with a normal ejection fraction.

BACKGROUND: Although heart failure with a preserved or normal ejection fraction (HFNEF or diastolic heart failure) is common, treatment outcomes on quality of life and cardiac function are lacking. The effect of renin-angiotensin blockade by irbesartan or ramipril in combination with diuretics on quality of life (QoL), regional and global systolic and diastolic function was assessed in HFNEF patients. METHODS: 150 patients with HFNEF (LVEF >45%) were randomised to (1) diuretics alone, (2) diuretics plus irbesartan, or (3) diuretics plus ramipril. QoL, 6-minute walk test (6MWT) and Doppler echocardiography were performed at baseline, 12, 24 and 52 weeks. RESULTS: The QoL score improved similarly in all three groups by 52 weeks (-46%, 51%, and 50% respectively, all p<0.01), although 6MWT increased only slightly (average +3-6%). Recurrent hospitalisation rates were equal in all groups (10-12% in 1 year). At 1 year, LV dimensions or LVEF had not changed in any group, though both systolic and diastolic blood pressures were lowered in all three groups from 4 weeks onwards. At baseline both mean peak systolic (Sm) and early diastolic (Em) mitral annulus velocities were reduced, and increased slightly in the diuretic plus irbesartan (Sm 4.5 (SEM 0.17) to 4.9 (SEM 0.16) cm/sec; Em 3.8 (SEM 0.25) to 4.2 (SEM 0.25) cm/sec) and ramipril (Sm 4.5 (SEM 0.24) to 4.9 (SEM 0.20) cm/sec; Em 3.3 (SEM 0.25) to 4.04 (SEM 0.32) cm/sec) groups (both p<0.05). NT-pro-BNP levels were raised at baseline (595 (SD 905) pg/ml; range 5-4748) and fell in the irbesartan (-124 (SD 302) pg/ml, p = 0.01) and ramipril (-173 (SD 415) pg/ml, p = 0.03) groups only. CONCLUSIONS: In this typically elderly group of HF patients with normal LVEF, diuretic therapy significantly improved symptoms and neither irbesartan nor ramipril had a significant additional effect. However, diuretics in combination with irbesartan or ramipril marginally improved LV systolic and diastolic longitudinal LV function, and lowered NT-proBNP over 1 year.

Tissue Doppler velocity is superior to displacement and strain mapping in predicting left ventricular reverse remodelling response after cardiac resynchronisation therapy.

OBJECTIVE: To compare the values of three different forms of tissue Doppler imaging (TDI) processing in predicting left ventricular (LV) reverse remodelling-namely, tissue velocity, displacement and strain mapping. DESIGN: Standard echocardiography with TDI was performed before and 3 months after cardiac resynchronisation therapy (CRT). SETTING: University teaching hospital. PATIENTS: 55 patients with heart failure who received CRT and were followed up for at least 3 months were recruited. INTERVENTIONS: During off-line analysis, the time to peak systolic velocity in the ejection phase, time to peak positive displacement and time to peak negative strain were measured in the six basal, six mid-segmental model. Parameters of systolic asynchrony derived by velocity, displacement and strain mapping were correlated with percentage reduction in LV end systolic volume (LVESV) and absolute gain in ejection fraction (EF). RESULTS: Among the three TDI processing technologies, all parameters of tissue velocity correlated with LV reverse remodelling (r = -0.49 to r = -0.76, all p < 0.001), but the predictive value was strongest in models with 12 LV segments. For displacement mapping, only the two parameters that included 12 LV segments correlated modestly with reduction in LVESV (r = -0.36, p < 0.05) and gain in EF. However, none of the strain mapping parameters predicted a favourable echocardiographic response. The receiver operating characteristic (ROC) curve areas were higher for parameters of tissue velocity based on 12 LV segments (ROC areas 0.88 and 0.94) than the corresponding areas derived from displacement mapping (ROC areas 0.72 and 0.71). CONCLUSION: Tissue velocity parameters of systolic asynchrony are superior to those of displacement and strain mapping in predicting LV reverse remodelling response after CRT.

Cardiovascular complications of severe acute respiratory syndrome.

BACKGROUND AND AIMS: Severe acute respiratory syndrome (SARS) is a virulent viral infection that affects a number of organs and systems. This study examined if SARS may result in cardiovascular complications. METHODS AND RESULTS: 121 patients (37.5 (SD13.2) years, 36% male) diagnosed to have SARS were assessed continuously for blood pressure, pulse, and temperature during their stay in hospital. Hypotension occurred in 61 (50.4%) patients in hospital, and was found in 28.1%, 21.5%, and 14.8% of patients during the first, second, and third week, respectively. Only one patient who had transient echocardiographic evidence of impaired left ventricular systolic function required temporary inotropic support. Tachycardia was present in 87 (71.9%) patients, and was found in 62.8%, 45.4%, and 35.5% of patients from the first to third week. It occurred independent of hypotension, and could not be explained by the presence of fever. Tachycardia was also present in 38.8% of patients at follow up. Bradycardia only occurred in 18 (14.9%) patients as a transient event. Reversible cardiomegaly was reported in 13 (10.7%) patients, but without clinical evidence of heart failure. Transient atrial fibrillation was present in one patient. Corticosteroid therapy was weakly associated with tachycardia during the second (chi(2) = 3.99, p = 0.046) and third week (chi(2) = 6.53, p = 0.01), although it could not explain tachycardia during follow up. CONCLUSIONS: In patients with SARS, cardiovascular complications including hypotension and tachycardia were common but usually self limiting. Bradycardia and cardiomegaly were less common, while cardiac arrhythmia was rare. However, only tachycardia persisted even when corticosteroid therapy was withdrawn.

Up-regulation of metallothionein isoforms in keloid keratinocytes.

Keloids are proliferative growths of dermal collagen, usually resulting from excessive tissue response during wound healing. There is evidence that keratinocytes may promote keloidogenesis via epithelial-mesenchymal interactions. Metallothioneins (MTs) are known to be involved in the fundamental cellular processes of growth and apoptosis. In this study, we evaluated the expression of MT isoforms in normal and keloid keratinocytes. The expression patterns of ten functional MT isoforms were assessed using real-time RT-PCR in primary cultures of normal and keloid keratinocytes. The MT-2A isoform was the most abundant MT isoform in both normal and keloid keratinocytes while the MT-1B isoform was absent. There was a significant increase in the mRNA expression of four MT isoforms, viz. MT-1A, 1E, 1F and 2A in keloid keratinocytes as compared to normal keratinocytes. Up-regulation of MT-1A, 1E, 1F and 2A isoforms may play a part in the development of keloids by paracrine signaling.

Chondroitin sulfate in palatal wound healing.

Chondroitin sulfate is up-regulated in granulation tissue during wound healing. To investigate the role of chondroitin sulfate in the wound-healing process after surgical repair of cleft palate, we isolated and cultured rabbit palatal fibroblasts. Treatment with chondroitin-6-sulfate resulted in a dose-dependent increase in cell adhesion and cell proliferation, whereas the reverse effects were seen after chondroitinase degradation of chondroitin sulfate. The biological actions of chondroitin sulfate appeared to be dependent on the presence and position of sulfate groups. Inhibition of glycosaminoglycan sulfation by chlorate treatment led to reduced cell adhesion and cell proliferation and a slower rate of wound closure in vitro. Furthermore, exposure to chondroitin-4-sulfate resulted in a dose-dependent reduction in cell adhesion. Together, these results show that chondroitin sulfate is involved in palatal wound healing.

Anti-ischemic action of estrogen-progestogen continuous combined hormone replacement therapy in postmenopausal women with established angina pectoris: a randomized, placebo-controlled, double-blind, parallel-group trial.

The benefit of treating postmenopausal women with established cardiovascular disease with combined estrogen-progestogen hormone replacement therapy (HRT) is controversial. This study investigated the effect of treatment with estradiol and norethisterone acetate on exercise tolerance and on the frequency and severity of ischemic attacks in postmenopausal women with stable angina pectoris. A total of 74 Chinese women were recruited for this 16-week double-blind, placebo-controlled trial. They were randomly allocated into two groups; one group received placebo/placebo/placebo and the other group received placebo/estrogen-progestogen/placebo. Estrogen-progestogen continuous combined HRT increased both time to 1-mm ST depression (99.1 s, p < 0.05) compared with a mean decrease of 22.9 s with placebo (p < 0.05), and total exercise duration also showed a significant increase (32.7 s, p < 0.05) after treatment compared with placebo (2.5 s, p < 0.05). In addition, the total number of ischemic events/24 h during ambulatory electrocardiographic monitoring decreased by 0.82 events after treatment (p < 0.05) compared with an increase in the placebo group (0.94), a highly significant difference (p = 0.006). These results suggest that the administration of this particular combined hormone replacement preparation may have a beneficial effect on myocardial ischemia in postmenopausal women with established coronary disease.

Lumbrical muscle with an additional origin in the forearm.

BACKGROUND: Although variations in the attachments of the lumbrical muscles have been commonly reported, these have been seen mainly in the Caucasian population. The present study is the first reported case of such an anomaly in a Chinese cadaver in the literature. METHODS: The upper extremities of 26 Chinese (23 male and three female) cadavers were examined. RESULTS: Dissection of a male 66-year-old Chinese cadaver has revealed the rare case of a bipennate first lumbrical muscle with an additional origin extending from the distal part of the forearm. Its first origin arose from the flexor digitorum profundus in the hand distal to the flexor retinaculum. The intrinsic muscles in the hands of all the other cadavers were normal. CONCLUSIONS: An anomalous origin of the lumbrical from muscles in the forearm has the potential to cause compression of the median nerve in the carpal tunnel.