How complex networks of activators and repressors lead to exquisitely specific cell type determination during development is poorly understood. In the Drosophila eye, expression patterns of Rhodopsins define at least eight functionally distinct though related subtypes of photoreceptors. Here, we describe a role for the transcription factor gene defective proventriculus (dve) as a critical node in the network regulating Rhodopsin expression. dve is a shared component of two opposing, interlocked feedforward loops (FFLs). Orthodenticle and Dve interact in an incoherent FFL to repress Rhodopsin expression throughout the eye. In the R7 and R8 photoreceptors, a coherent FFL relieves repression by Dve while activating Rhodopsin expression. Therefore, this network uses repression to restrict, and combinatorial activation to induce cell type-specific expression. Further, Dve levels are finely tuned to yield cell type- and region-specific repression or activation outcomes. This interlocked FFL motif may be a general mechanism to control terminal cell fate specification.

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lectrocardiographic (ECG) and echocardiographic examinations are 2 major tools for the identification of patients with hypertrophic cardiomyopathy (HCM). In almost all patients with HCM, echocardiography is more valuable not only for the diagnosis of the disease but also for the localization and the quantification of the hypertrophy when left ventricular hypertrophy (LVH) and ST-T abnormalities with or without abnormal Q waves are present on ECG. It is well known that asymmetric septal hypertrophy is the most common feature, 1 but many subgroups 2 or other forms of hypertrophy, such as apical, 3,4 symmetric, 5,6 or reversed posterior hypertrophy, 7 have been reported in the literature.In our daily practice, we occasionally encounter patients with ECG evidence of LVH that cannot be explained even with other invasive or noninvasive examinations. We recognized that in some of these patients, the papillary muscles of the left ventricle were hypertrophied on echocardiography, but no other hypertrophic segment could be detected. We also found this papillary muscle hypertrophy in the relatives of the patients with typical HCM in a family survey using echocardiography. Therefore, this present study was performed to examine whether solitary papillary muscle hypertrophy of the left ventricle is a new subtype of or an early form of HCM. Japanese Circulation Journal Vol.62, November 1998 Methods EchocardiographyTwo-dimensional echocardiographic observations were made via the transthoracic approach in the left lateral decubitus position with a 3.75 MHz transducer using a Toshiba SSH-140A or 160A apparatus (Toshiba Medical Co, Tokyo, Japan). When the visualization via the transthoracic approach was poor, echocardiographic evaluation was performed by the transesophageal approach with a 5 MHz transesophageal echocardiographic probe (Model PEF-507SB, Toshiba Medical Co) using the same apparatus. Definition of Papillary Muscle HypertrophyAt present, there are no data concerning the size of the papillary muscle in normal subjects. Therefore, we determined the normal size of the papillary muscle by conducting an echocardiographic study in 40 healthy volunteers (23 males and 17 females, age range, 15-77 years) who showed normal physical and ECG findings. From the parasternal view of the transverse section of the left ventricle, where the bases of the papillary muscles were clearly visualized as circles and the muscles probably had their maximum sizes, the horizontal and vertical diameters of the anterolateral and posteromedial papillary muscles were measured at end-diastole. The horizontal diameter was measured in parallel with a line drawn between the centers of the anterolateral and posteromedial papillary muscles, and the vertical diameter perpendicularly to it (Fig 1). In the 3 patients whose left ventricles were poorly visualized on the parasternal approach, the measurements were made similarly but using the transgastric short-axis view via the Jpn Circ J 1998; 62: 811 -816 (Received May 6, 1998; revised manuscript received Ju...

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The purpose of the present study was to determine whether parameters of left atrial appendage (LAA) function, assessed by transesophageal echocardiography (TEE), could predict the clinical outcome in patients with dilated cardiomyopathy (DCM). Fifty-five patients (20 had ischemic cardiomyopathy; mean age, 56+/-14 years) who underwent TEE to evaluate LAA function from 1992 to 1996 were studied. After a mean follow-up period of 34+/-13 months, 16 patients died; the cause was cardiac in 14 and noncardiac in 2. Patients who died of cardiac cause had a lower LAA emptying velocity than survivors (38+/-18 vs 54+/-18 cm/s, p=0.01). There were, however, no significant differences between survivors and nonsurvivors with regard to the maximal LAA area (4.3+/-1.3 vs 4.5+/-0.9 cm2, p=0.55), minimal LAA area (2.4+/-1.1 vs 2.9+1.1 cm2, p=0.13), and LAA ejection fraction (46+/-16 vs 36+/-18%, p=0.05). On the Cox proportional hazards model analysis, LAA emptying velocity <50 cm/s (chi-square 5.9, p=0.02), LAA ejection fraction <43% (chi-square 5.6, p=0.02), female gender (chi-square 5.2, p=0.02), pulmonary artery wedge pressure > or =14 mmHg (chi-square 4.8, p=0.03), E/A ratio > or =1.3 (chi-square 4.6, p=0.03), deceleration time <148 ms (chi-square 4.6, p=0.03), and cardiothoracic ratio > or =54% (chi-square 4.3, p=0.04) were significantly related to cardiac death. The stepwise multivariate analysis revealed that LAA emptying velocity (chi-square 6.1, p=0.01) and gender (chi-square 5.4, p=0.02) were the independent predictors for outcome. In conclusion, the parameters of LAA function may be useful predictors of the clinical outcome in patients with DCM.

We prospectively examined the relationship between pulmonary venous flow velocity determined by transesophageal echocardiography and pulmonary capillary wedge pressure (PCWP) determined with a Swan-Ganz catheter in 40 consecutive patients who were all in sinus rhythm and without significant mitral valve disease. Correlations were assessed between the four components of pulmonary venous flow – atrial reversal flow (A), early systolic (SI) and late systolic (S2) forward flow, and diastolic forward flow (D) – and PCWP. Multiple regression analysis showed that PCWP could be estimated from only two (S2 and D) among these four components. Thus, PCWP was estimated by using the following equation with a strong correlation (r = 0.83) to measured one by catheterization: PCWP = –0.07 × S2+0.27 × D+2.3 mm Hg. In addition, prospective estimation of PCWP by this equation in an additional 25 patients gave a good correlation with the measured values (r = 0.83). PCWP can be estimated by our new equation using the peak velocity of late systolic forward and diastolic forward flow in pulmonary vein in patients with various types of heart diseases.