Faculty Bibliography

OBJECTIVES: To assess the safety and efficacy of laparoscopic ablation of symptomatic renal cysts as minimally invasive therapeutic techniques have largely supplanted open surgical intervention for the treatment of symptomatic renal cysts. METHODS: The records of 32 consecutive adult patients who underwent laparoscopic ablation of renal cysts (11 peripelvic, 21 parenchymal) were retrospectively reviewed. All patients were symptomatic at presentation; 26 had a single cyst, 5 had two cysts, and 1 had four cysts. RESULTS: Twenty patients underwent a transperitoneal laparoscopic approach, and 12 patients underwent a retroperitoneal laparoscopic approach. An average of 3.2 ports were used for each procedure, and no open conversions or transfusions were necessary. When comparing patients with parenchymal and peripelvic cysts, statistically significant differences were noted in the mean operative time (164 versus 233 minutes, respectively; P = 0.003) and mean operative blood loss (98 versus 182 mL, respectively; P = 0.04). Four patients (13%) had complications (one major and three minor), including a persistent ureteral stricture. One patient with negative preoperative aspiration cytology and negative intraoperative frozen section analysis was later found to have malignancy within the cyst wall, necessitating radical nephrectomy and trocar site excision. One patient (3%) developed a recurrence. CONCLUSIONS: Laparoscopic ablation of symptomatic renal cysts is a safe and efficacious procedure. We report an overall complication rate of 13% and a recurrence rate of 3% with a mean follow-up of 18.1 months (median 10.0).

Ectropion, or eversion of the lid margin away from the globe, can occur after surgical reconstruction of facial defects that encroach on the lower eyelid. This article discusses prevention of ectropion in the reconstruction of facial defects

It is unclear whether cleft palate formation is attributable to intrinsic biomolecular defects in the embryonic elevating palatal shelves or to an inability of the shelves to overcome a mechanical obstruction (such as the tongue in Pierre Robin sequence) to normal fusion. Regardless of the specific mechanism, presumably embryonic palatal shelves are ultimately unable to bridge a critical distance and remain unapproximated, resulting in a clefting defect at birth. We propose to use a palate organ culture system to determine the critical distance beyond which embryonic palatal shelves fail to fuse (i.e., the minimal critical intershelf distance). In doing so, we hope to establish an in vitro cleft palate model that could then be used to investigate the contributions of various signaling pathways to cleft formation and to study novel in utero treatment strategies.Palatal shelves from CD-1 mouse embryos were microdissected on day 13.5 of gestation (E13.5; term = 19.5 days), before fusion. Using a standardized microscope ocular grid, paired palatal shelves were placed on a filter insert at precisely graded distances ranging from 0 (in contact) to 1.9 mm (0, 0.095, 0.19, 0.26, 0.38, 0.48, 0.57, 0.76, 0.95, and 1.9 mm). A total of 68 paired palatal shelves were placed in serum-free organ culture for 96 hours (n = 68). Sample sizes of 10 were used for each intershelf distance up to and including 0.48 mm (n = 60). For intershelf distances of 0.57 mm and greater, two-paired palatal shelves were cultured (n = 8). All specimens were assessed grossly and histologically for palatal fusion.Palatal fusion occurred in our model only when intershelf distances were 0.38 mm or less. At 0.38 mm, eight of 10 palates appeared grossly adherent, whereas six of 10 demonstrated clear fusion histologically with resolution of the medial epithelial seam and continuity of the palatal mesenchyme. None of the 18 palates fused when placed at intershelf distances of 0.48 mm or greater.Using our selected intershelf distances as a guideline, we have established an approximate minimal critical intershelf distance (0.48 mm) at which we can reliably expect no palatal fusion. Culturing palatal shelves at intershelf distances of 0.48 mm or greater results in nonfusion or clefting in vitro. This model will allow us to study biomolecular characteristics of unfused or cleft palatal shelves in comparison with fused shelves. Furthermore, we plan to study the efficacy of grafting with exogenous embryonic mesenchyme or candidate factors to overcome clefting in vitro as a first step toward future in utero treatment strategies

OBJECTIVE: Two possible explanations for an hypothesized association between depression and hypertension were examined: (1) shared stress-related risk factors are associated with both depression and hypertension and (2) life-style factors associated with depression lead to hypertension. METHODS: A predominantly black sample of 695 adults were interviewed in the Harlem Household Survey. Two measures of hypertension were used and compared-1) self-report and 2) elevated blood pressure (above 140/90 mm Hg)-on the basis of the mean of two blood pressure measures. Depressive symptoms were measured by use of a 24-item scale based on the Diagnostic Interview Schedule. Logistic regression models were used to test associations between hypertension and depressive symptoms, stressors, and life-style factors. RESULTS: Depressive symptoms were associated with self-reported hypertension but not with elevated blood pressure. The association between self-reported hypertension and depressive symptoms was explained partly by shared stress-related risk factors but not by life-style factors. Several stressors and life-style variables were risk factors for elevated blood pressure independently of depressive symptoms. The findings are consistent with studies that have measured hypertension variously by either self-report or blood pressure. Possible explanations were explored (labeling and help-seeking) but were not supported by the data. CONCLUSIONS: An association was found between self-reported hypertension and depressive symptoms, which was explained partly by shared stress-related risk factors. Elevated blood pressure was associated with stressors and life-style factors but not with depressive symptomatology. Research on illness representations and cultural dimensions of health suggest avenues for further investigation.

The majority of adult brachial plexus palsies are posttraumatic injuries caused by high-energy forces, usually involving motor vehicles. In infants, brachial plexus palsies commonly represent obstetrical injuries following excessive traction on the plexus during complex or difficult delivery. Most adult injuries, and occasionally those in infants, represent brachial plexus root avulsion injuries that carry serious ramifications from the standpoint of permanent disability of a paralyzed extremity, prolonged recuperation, and significant socioeconomic impact. Modern-day management of root avulsions should focus on early, aggressive microsurgical reconstruction of the brachial plexus, combining various neurotizations with intraplexus and extraplexus ipsilateral and contralateral nerve donors, utilization of vascularized nerve grafts, and finally the use of free vascularized and neurotized muscles. When these multistage microsurgical management techniques are applied early (with complete avulsions) they may often result in significant return of neurologic function, especially in young patients. Amputation should be looked upon as an option only when these newer microsurgery techniques have failed

Facial paralysis (FP) remains today one of the most disturbing cranial nerve disorders. The present study utilized the rat model of FP and examined a dual approach of combining the current microsurgical treatment of cross-facial nerve graft (CFNG) with local administration of insulin-like growth factor-I (IGF-I). The efficacy of this combined treatment approach was assessed by motor end-plate analysis of the reinnervated orbicularis oculi muscle (OOM). Local administration of IGF-I (50 microg/ml) to the CFNG demonstrated a 61 percent increase in the number of end-plates in the reinnervated OOMs, compared to the OOMs reinnervated with CFNG plus vehicle. These results indicate that the local therapeutic augmentation of IGF-I levels at the coaptation site(s) of the CFNG may, in fact, enhance reinnervation of muscle and recovery of function in general

Vascular disruption secondary to fracture creates a hypoxic gradient of injury wherein the oxygen tension at the center of the wound is very low. In vivo this hypoxic microenvironment stimulates the expression of a variety of cytokines from inflammatory cells, fibroblasts, endothelial cells, and osteoblasts. In order to begin to dissect this complex system, we have examined the effects of hypoxia on isolated osteoblast gene expression in vitro. Understanding gene expression in this system may facilitate the development of targeted therapeutic modalities designed to accelerate fracture repair and reduce complications. Using an established model of in vitro hypoxia, we have analyzed the expression of genes involved in bone matrix production and turnover. Subconfluent neonatal rat calvarial osteoblasts were exposed to hypoxia (pO(2) = 35-40 mm Hg) and total cellular RNA was collected at 0, 3, 6, 24, and 48 h. Northern analysis was used to analyze the expression patterns of (1) transforming growth factors (TGFs)-beta1, -beta2, and -beta3 and their type I receptor; (2) collagens I and III; and (3) tissue inhibitor of metalloproteinase-1. We have demonstrated a marked elevation of TGF-beta1 gene expression within 3 h of hypoxia. Although neither TGF-beta2 nor TGF-beta3 expression was affected by hypoxia, the TGF-beta type I receptor was substantially upregulated within 6 h. In addition, extracellular matrix scaffolding molecules (collagens I and III) were markedly, but differentially, upregulated. Finally, we have demonstrated that the expression of an inhibitor of extracellular matrix turnover, the tissue inhibitor of metalloproteinase-1, was strikingly decreased in response to hypoxia. These results imply that hypoxia can affect osseous healing by altering the expression of cytokines, bone-specific extracellular matrix molecules, and their regulators