Partial Arrest Research Articles

Surgical exposure of turner’s tooth and CBCT representation of inverted tooth: A case report

Enamel defects related to it’s thickness and quality are called hypoplasia, and they arise from disturbances in the enamel matrix development process. The possible developmental disruptions, which can range from mild changes in enamel mineralization to severe sequestration of the tooth germ, dilations of the crown or root, crown or root duplication, and complete or partial arrest of root formation, are explained by the topographic relationship between the primary tooth and the developing permanent tooth germ. Enamel in Turner's hypoplastic kinds might be shiny, rough, or pitted . It is extremely uncommon for permanent central incisor impaction and inversion to result from trauma, odontomas, and neighboring supernumerary teeth. Root development is restricted when incisors are displaced or impacted in the opposite direction. Dental radiographs and CBCT are used to assess the presence or absence of enamel thickening and inversion. This information is used not only for diagnosis but also to build the best possible treatment plan. Hence a case is presented of Turner’s hypoplasia and maxillary lateral incisor inversion in a 9 yr old female. MESH- Turner’s Hypoplasia, Tooth inversion, CBCT, RVG

The effect of silver diammine fluoride on In Vitro Enamel caries lesion remineralization and staining as a function of lesion baseline mineral distribution

Objectivesto investigate whether baseline mineral distribution modulates the ability of silver diammine fluoride (SDF) to remineralize and stain enamel caries lesions. MethodsThis laboratory study followed a 3 [treatment: SDF/fluoride varnish (FV)/deionized water (DIW)] ×3 [lesion protocol: methylcellulose (MeC)/hydroxyethylcellulose (HEC)/Carbopol 907 (C907)] factorial design. Lesions were created in bovine enamel specimens (n = 20). Treatments were applied and lesions remineralized in artificial saliva. Digital transverse microradiography (TMR-D) was used to analyze lesions. Lesion color was monitored spectrophotometrically. The effects of lesion protocol and treatment on changes in lesion depth (ΔLD), mineral loss (ΔΔZ), maximum mineral density at the surface zone (ΔSZmax), and color changes related to remineralization (ΔL*remin) were analyzed using two-way ANOVA. ResultsThe treatment×lesion protocol interaction was significant for ΔΔZ (p < 0.01) and ΔL*remin (p < 0.01), however not for ΔLD (p = 0.23) or ΔSZmax (p = 0.91). There were no differences in ΔΔZ between treatments in HEC and C907 lesions. However, DIW resulted in more remineralization than both SDF (p < 0.01) and FV (p = 0.01) in MeC lesions. Considering changes from lesion baseline after remineralization in MeC lesions, SDF treatment resulted in the highest mineral gain in the surface zone. However, DIW revealed the highest mineral gain after remineralization in the lesion body. SDF stained lesions with the intensity increasing after remineralization in C907 lesions, whereas staining decreased in MeC and HEC lesions. ConclusionHigh fluoride treatments can interfere with continuous remineralization of caries lesions due to partial arrest. Baseline lesion mineral distribution affects SDF's ability to enhance remineralization and the staining caused by SDF. Clinical SignificanceSDF is being used to arrest active caries lesions extending into dentin and to treat dentin hypersensitivity. This study shed light on SDF's effect on an isolated process in dental caries only, remineralization. It achieved this by examining enamel caries lesions with differing mineral distributions and assessing their staining properties.

Numerical analysis of 3D nonplanar hydraulic fracture propagation in fractured-vuggy formations using a hydromechanical coupled XFEM approach

In this paper, a hydromechanical coupled XFEM approach is developed for simulating 3D nonplanar hydraulic fracturing, fracture–vug interactions and natural crack intersection problems. The extended finite element method associated with a high-order tip enrichment function is used for describing rock deformation, and the finite element method is chosen for discretizing fluid flow at the fracture surface. Rock deformation and fluid flow are coupled and solved by the Picard iteration method. The hybrid explicit–implicit representation method is adopted to represent 3D nonplanar fracture surfaces, and the displacement correlation method is chosen for extracting the mixed-mode stress intensity factor. A new mixed-mode failure criterion is introduced for determining 3D nonplanar fracture growth. Analytical solutions and experimental investigations are employed to verify the validity and effectiveness of our model. The simulations of fracture–vug interactions show that fracture surface growth on the side without vugs is constrained, while vugs can aggravate the tortuousness of the fracture surface on the side with vugs. In addition, four new intersection patterns (penetration, partial arrest, partial diversion, full arrest, and vertical propagation) are found in the 3D nonplanar fracture intersection simulations. The numerical examples highlight the considerable impacts of vertical growth and the mixed-mode effect on hydraulic fracturing.

Surfeit locus protein 4 modulates endoplasmic reticulum function and maintains oocyte quality

ABSTRACT Surfeit locus protein 4 is a cargo receptor mediating cargo transport from the endoplasmic reticulum lumen to the Golgi apparatus. Loss of Surf4 gene led to embryonic lethality in mice. However, the role of Surf4 during oocyte development remains unknown. In this study, we generated the mouse model with oocyte-specific knockout of Surf4 gene. We found that adult mice with deletion of Surf4 showed normal folliculogenesis, ovulation and fertility. However, loss of Surf4 slightly impaired oocyte quality, thus led to partial oocyte meiotic arrest and reduced ratio of blastocyst formation. Consistent with this, the distribution of endoplasmic reticulum was disturbed in Surf4-deficient oocytes in mice. These results demonstrated that although Surf4 is dispensable for female mouse fertility, Surf4 modulates endoplasmic reticulum arrangement and participates in regulation of developmental competence of oocytes.

An Update on the Genetics of Polycystic Ovary Syndrome

PCOS is a common endocrinopathy among women of reproductive age, with a worldwide prevalence of 8 to 13%, depending on the criteria used for diagnosis. It is characterized by a constellation of features, including oligo/anovulation, clinical and/or biochemical hyperandrogenism, and polycystic ovarian morphology. PCOS is one of the common causes of female infertility. It is also associated with metabolic derangements, including obesity, insulin resistance, and compensatory hyperinsulinemia, which increase the likelihood of developing type 2 diabetes mellitus. Despite extensive research, the etiology of PCOS remains largely unknown. It seems likely that the hypothalamic-pituitary-ovarian axis dysfunction, partial folliculogenesis arrest, insulin resistance, and ovarian and adrenal androgen secretion may play a role in the pathogenesis of PCOS. Familial clustering of the cases of PCOS points to a genetic component linked with it. The initial genetic studies suggest an autosomal dominant pattern of inheritance of the disorder in some families; however, most studies support multifactorial origin. Since PCOS is a complex trait, the typical form of inheritance of PCOS follows a non-Mendelian pattern and involves complex genetic mechanisms. Studies involving linkage and association have suggested a connection between genetic variations and the risk of developing PCOS in certain families or populations. Through genome-wide association studies and next-generation sequencing techniques, several candidate genes have been identified that play a role in the etiopathogenesis of the disorder. Pathogenic variants of various genes such as INSR, IRS1, GHRL, LDLR, MC4R, ADIPOQ, UCP1, UCP2, UCP3, FTO, PCSK9, FBN3, NEIL2, FDFT1, PCSK9, CYP11, CYP17, CYP21, HSD17, STAR, POR, AKR1C3, AMH, AMHR2, INHBA, AR, SHBG, LHR, FSHR, FSH β, SRD5A, GATA4, THADA, YAP1, ERBB2, DENND1A, FEM1B, FDFT1, NEIL2, TCF7L2, etc. in some PCOS cases are linked as underlying etiologic associations. This review aims to provide insight into the current genetic knowledge about PCOS. Discovering the genetic factors and pathways involved in the disorder will help us better comprehend the underlying mechanisms of the disorder.

Physeal bar resection by modified arthroscopically assisted surgery in a closed osteocavity.

Physeal bar resection has been used for partial growth arrest treatment for a decade while removing the bony bar minimally invasively and accurately is challenging. This research aims to illustrate a modified arthroscopically assisted surgery, by which all the procedure was under all-inside visualization, without the constant exchange between burring under fluoroscopy, followed by irrigation, suction, and arthroscopy of the canal. We retrospectively reviewed the patients who sustained physeal bar resection under direct all-inside visualization of the arthroscope during 2016-2021. Patients who underwent physeal bar resection with the aid of an arthroscope for identifying the physeal cartilage but not resecting and visualizing the physeal bar simultaneously were excluded from this study. In total, nine patients with ten related joints were included in this study. All the patients were followed up for at least two years. The average following time was 28.5 ± 6.7 months. Eight patients with nine related joints had an improvement of angular deformity, averaging 8.3 ± 6.9 degrees, and one had a worsening of the angular deformity. All the patients had a leg length discrepancy improvement, while four patients still had LLD >1 cm. The surgery time was 3.1 ± 0.7 h. There were no postoperative fractures, infections, or intraoperative complications such as neurovascular injury. Using clamps to form a closed osteocavity could make physeal bar resection under all-inside arthroscopic visualization feasible, which is minimally invasive, accurate, and safe.

Surgical Correction of Posttraumatic Varus Deformity of the Distal Tibia Due to Medial Growth Arrest in Children and Adolescents: Surgical Technique

Background: Varus deformity of the distal tibia secondary to epiphyseal fracture and partial growth arrest is relatively common. Growth arrest of the medial part of the epiphysis leads to varus deformity of the distal tibia and fibular overgrowth. If the deformity is left untreated, the malalignment may lead to irreversible damage and early ankle joint osteoarthritis in the long term. Several surgical techniques have been described in the literature to achieve correction and prevent late complications. These include the closure of the remaining epiphysis and various osteotomies around the ankle, using internal and external fixation. Materials and Methods: We report a technique that includes medial open wedge supramalleolar osteotomy, insertion of a structural cortical allograft and fixation with an anatomically contoured locking plate, completion of closure of the distal tibial physis, and distal fibular epiphysiodesis to prevent tibiofibular relations distortion. Part of this protocol is osteotomy of the distal fibula to prevent excessive pressure on the talus, and at the end of the operation, fibular fixation should be performed as well. In children with open physis and potential for significant leg length discrepancy, we recommend closure of the contralateral physis of the distal tibia and fibula. To the best of our knowledge, precise details of this protocol have not been described. Conclusion: We believe that this protocol is a reliable, accurate, and relatively simple method that provides not only anatomic correction and restoration of the ankle joint to prevent early ankle and subtalar arthritis but also addresses late complications, such as ipsilateral fibular overgrowth and limb length discrepancy.

The regenerative treatment of costal osteochondral graft implantation for partial growth arrest using a rabbit model

PurposeTo investigate the feasibility of cylindrical costal osteochondral graft transplantation as a novel regenerative treatment in growth arrest. MethodsThe medial portion of the proximal tibial growth plate of 6-week-old male New Zealand White rabbits was resected to establish an experimental model of partial growth plate injury. The rabbits were divided into four groups: no-treatment, bone wax transplantation, costal chondral graft, and costal osteochondral graft groups. Radiographic and micro-computed tomography scan results were analyzed to evaluate angular deformity of the tibia and bony bridge formation at the injury site. In addition, repair of the injured growth plate cartilage was assessed histologically at 4, 8, and 12 weeks postoperatively. ResultsRadiographic examination revealed that bone wax transplantation continuously decreased the medial proximal tibial angle (MPTA) while the costal chondral graft implantation reduced the decrease of MPTA at 12 weeks postoperatively. The costal osteochondral graft implantation recovered the MPTA, close to the normal. Histologically, the costal osteochondral grafts retained the MPTA in the injured site compared to costal chondral grafts. Additionally, hypertrophic chondrocytes were observed at the graft site in the costal osteochondral graft group at 12 weeks, suggesting that endochondral ossification may occur at the graft site similar to normal ossification. The fluorescence in situ hybridization analysis of osteochondral grafts transplanted from male to female rabbits indicated that they were replaced by cells of host origin. ConclusionThe costal osteochondral graft can achieve regeneration without bony bridge formation in partial growth plate injury.

The effectiveness of physeal bar resection with or without Hemi-Epiphysiodesis to treat partial growth arrest

PurposeTo evaluate the outcomes of distal femoral, proximal tibial, and distal tibial physeal bar resection combined with or without the Hemi-Epiphysiodesis procedure and provide a better understanding of the application of physeal bar resection combined with Hemi-Epiphysiodesis procedure in the treatment of physeal bar growth arrest.MethodsWe retrospectively reviewed the patients who suffered physeal bar and underwent physeal bar resection with or without the Hemi-Epiphysiodesis technique during 2010–2020. All were followed up for at least 2 years or to maturity. A modified mapping method was used to determine the area of a physeal bar by CT data. The aLDFA, aMPTA, aLDTA, MAD, and LLD were measured to assess the deformity of the lower limb.ResultsIn total, 19 patients were included in this study. The average age was 8.9 years (range 4.4 to 13.3 years old). During the follow-up, 4 (21.1%) patients had an angular change < 5°; 12 (63.2%) patients had angular deformity improvement > 5° averaging 10.0° (range 5.3° to 23.2°), and 3 (15.8%) patients had improvement of the angular deformity averaging 16.8° (range 7.4° to 27.1°). Eleven patients (57.9%) had significant MAD improvement. After surgery, we found that 7 (36.8%) patients had an LLD change of < 5 mm and were considered unchanged. Only 2 (15%) patients had an LLD improvement > 5 mm averaging 1.0 cm (range 0.7 to 1.3 cm), and 7 (36.8%) patients had increasing of LLD > 5 mm averaging 1.3 cm (range 0.5 to 2.5 cm). There were no postoperative fractures, infections, or intraoperative complications such as neurovascular injury.ConclusionPhyseal bar resection combined with Hemi-epiphysiodesis is helpful for partial epiphysis growth arrest. Without statistically verifying, we still believe that patients with limited growth ability could benefit more from physeal bar resection combined with Hemi-epiphysiodesis.

Comprehensive semen examination in patients with pancreatic-sufficient and pancreatic-insufficient cystic fibrosis.

We examined a cohort of 93 cystic fibrosis (CF) male patients who were pancreatic-sufficient (PS-CF; n=40) or pancreatic-insufficient (PI-CF; n = 53). Complex semen examination was performed, including standard semen analysis, quantitative karyological analysis (QKA) of immature germ cells (IGCs), transmission electronic microscopy (TEM), biochemical analysis, and sperm DNA fragmentation by terminal deoxynucleotidyl transferase-mediated dUTP nickend labeling (TUNEL) assay. Azoospermia was diagnosed in 83 (89.2%) patients. The other 10 (10.8%) patients were found to be nonazoospermic and showed various spermatological diagnoses (asthenozoospermia, n = 2; asthenoteratozoospermia, n = 3; oligoasthenozoospermia, n = 1; oligoasthenoteratozoospermia, n = 3; and normozoospermia, n = 1) with no specific morphological abnormalities. Oligospermia was detected in 89.2% azoospermic and 30.0% nonazoospermic patients. Low seminal pH (<7.0) was found in 74 (89.2%) of 83 azoospermic patients. Moderate leukocytospermia (2.0 × 10 6 -2.2 × 10 6 ml -1 ) was revealed in 2.4% azoospermic and 40.0% nonazoospermic semen samples. The signs of partial meiotic arrest at prophase I were found in 4 of 6 nonazoospermic patients examined by QKA of IGCs. The content of fructose and citrate was low in oligospermic and normal in nonoligospermic semen samples. An increased percentage (>30%) of spermatozoa with noncondensed ("immature") chromatin was revealed in 2 of 6 nonazoospermic semen samples analyzed by TEM.

Loss of function of membrane estrogen receptor ERα alters expansion of trophoblast cells and impacts mouse fertility

17β-estradiol following binding to estrogen receptor alpha (ERα) exerts a critical role in the control of reproduction, acting through both nuclear and membrane-initiated signaling. To study the physiological role of membrane ERα in the reproductive system, we used the C451A-ERα mouse model with selective loss-of-function of membrane ERα. Despite C451A-ERα mice being described as sterile, daily weighing and ultrasound imaging revealed that homozygous females do get pregnant, allowing to investigate the role of ERα during pregnancy for the first time. Total neonatal deaths of the mice offspring resulted from delayed parturition associated with failure in pre-term progesterone withdrawal. Moreover, pregnant C451A-ERα females exhibit partial intrauterine embryo arrest at about E9.5. The observed embryonic lethality results from altered expansion of Tpbpa-positive spiral artery-associated trophoblast giant cells (SpA-TGCs) into the utero-placental unit, associated with the imbalance expression of angiogenic factors, together controlling the trophoblast-mediated spiral arterial remodeling. Hence, maternal loss of membrane ERα function clearly alters the activity of invasive trophoblast cells during placentogenesis. This novel function of membrane ERα could open new avenues towards a better understanding of human pregnancy-associated pathologies.

Oocyte-Specific Knockout of Histone Lysine Demethylase KDM2a Compromises Fertility by Blocking the Development of Follicles and Oocytes.

The methylation status of histones plays a crucial role in many cellular processes, including follicular and oocyte development. Lysine-specific demethylase 2a (KDM2a) has been reported to be closely associated with gametogenesis and reproductive performance, but the specific function and regulatory mechanism have been poorly characterized in vivo. We found KDM2a to be highly expressed in growing follicles and oocytes of mice in this study. To elucidate the physiological role of Kdm2a, the zona pellucida 3-Cre (Zp3-Cre)/LoxP system was used to generate an oocyte Kdm2a conditional knockout (Zp3-Cre; Kdm2aflox/flox, termed Kdm2a cKO) model. Our results showed that the number of pups was reduced by approximately 50% in adult Kdm2a cKO female mice mating with wildtype males than that of the control (Kdm2aflox/flox) group. To analyze the potential causes, the ovaries of Kdm2a cKO mice were subjected to histological examination, and results indicated an obvious difference in follicular development between Kdm2a cKO and control female mice and partial arrest at the primary antral follicle stage. The GVBD and matured rates of oocytes were also compromised after conditional knockout Kdm2a, and the morphological abnormal oocytes increased. Furthermore, the level of 17β-estradiol of Kdm2a cKO mice was only 60% of that in the counterparts, and hormone sensitivity decreased as the total number of ovulated and matured oocytes decreased after superovulation. After deletion of Kdm2a, the patterns of H3K36me2/3 in GVBD-stage oocytes were remarkedly changed. Transcriptome sequencing showed that the mRNA expression profiles in Kdm2a cKO oocytes were significantly different, and numerous differentially expressed genes were involved in pathways regulating follicular and oocyte development. Taken together, these results indicated that the oocyte-specific knockout Kdm2a gene led to female subfertility, suggesting the crucial role of Kdm2a in epigenetic modification and follicular and oocyte development.

Loss of function of the maternal membrane oestrogen receptor ERα alters expansion of trophoblast cells and impacts mouse fertility.

The binding of 17β-oestradiol to oestrogen receptor alpha (ERα) plays a crucial role in the control of reproduction, acting through both nuclear and membrane-initiated signalling. To study the physiological role of membrane ERα in the reproductive system, we used the C451A-ERα mouse model with selective loss of function of membrane ERα. Despite C451A-ERα mice being described as sterile, daily weighing and ultrasound imaging revealed that homozygous females do become pregnant, allowing the investigation of the role of ERα during pregnancy for the first time. All neonatal deaths of the mutant offspring mice resulted from delayed parturition associated with failure in pre-term progesterone withdrawal. Moreover, pregnant C451A-ERα females exhibited partial intrauterine embryo arrest at about E9.5. The observed embryonic lethality resulted from altered expansion of Tpbpa-positive spiral artery-associated trophoblast giant cells into the utero-placental unit, which is associated with an imbalance in expression of angiogenic factors. Together, these processes control the trophoblast-mediated spiral arterial remodelling. Hence, loss of membrane ERα within maternal tissues clearly alters the activity of invasive trophoblast cells during placentogenesis. This previously unreported function of membrane ERα could open new avenues towards a better understanding of human pregnancy-associated pathologies.

Insights into the developing fovea revealed by imaging.

Early development of the fovea has been documented by histological studies over the past few decades. However, structural distortion due to sample processing and the paucity of high-quality post-mortem tissue has limited the effectiveness of this approach. With the continuous progress in high-resolution non-invasive imaging technology, most notably optical coherence tomography (OCT) and OCT angiography (OCT-A), in vivo visualization of the developing retina has become possible. Combining the information from histologic studies with this novel imaging information has provided a more complete and accurate picture of retinal development, and in particular the developing fovea. Advances in neonatal care have increased the survival rate of extremely premature infants. However, with enhanced survival there has been an attendant increase in retinal developmental complications. Several key abnormalities, including a thickening of the inner retina at the foveal center, a shallower foveal pit, a smaller foveal avascular zone, and delayed development of the photoreceptors have been described in preterm infants when compared to full-term infants. Notably these abnormalities, which are consistent with a partial arrest of foveal development, appear to persist into later childhood and adulthood in these eyes of individuals born prematurely. Understanding normal foveal development is vital to interpreting these pathologic findings associated with prematurity. In this review, we first discuss the various advanced imaging technologies that have been adapted for imaging the infant eye. We then review the key events and steps in the development of the normal structure of the fovea and contrast structural features in normal and preterm retina from infancy to childhood. Finally, we discuss the development of the perifoveal retinal microvasculature and highlight future opportunities to expand our understanding of the developing fovea.

Axin2/Conductin Is Required for Normal Haematopoiesis and T Lymphopoiesis.

The development of T lymphocytes in the thymus and their stem cell precursors in the bone marrow is controlled by Wnt signaling in strictly regulated, cell-type specific dosages. In this study, we investigated levels of canonical Wnt signaling during hematopoiesis and T cell development within the Axin2-mTurquoise2 reporter. We demonstrate active Wnt signaling in hematopoietic stem cells (HSCs) and early thymocytes, but also in more mature thymic subsets and peripheral T lymphocytes. Thymic epithelial cells displayed particularly high Wnt signaling, suggesting an interesting crosstalk between thymocytes and thymic epithelial cells (TECs). Additionally, reporter mice allowed us to investigate the loss of Axin2 function, demonstrating decreased HSC repopulation upon transplantation and the partial arrest of early thymocyte development in Axin2Tg/Tg full mutant mice. Mechanistically, loss of Axin2 leads to supraphysiological Wnt levels that disrupt HSC differentiation and thymocyte development.

A Systematic Review of the Impact of Mitochondrial Variations on Male Infertility.

According to current estimates, infertility affects one in four couples trying to conceive. Primary or secondary infertility can be due either to both partners or only to the man or the woman. Up to 15% of infertility cases in men can be attributed to genetic factors that can lead to irreversible partial or complete spermatogenic arrest. The increased use of assisted reproductive technology (ART) has provided not only insights into the causes of male infertility but also afforded a diagnostic tool to detect and manage this condition among couples. Genes control a variety of physiological attributes, such as the hypothalamic–pituitary–gonadal axis, development, and germ cell differentiation. In the era of ART, it is important to understand the genetic basis of infertility so as to provide the most tailored therapy and counseling to couples. Genetic factors involved in male infertility can be chromosome abnormalities or single-gene disorders, mitochondrial DNA (mtDNA) mutations, Y-chromosome deletions, multifactorial disorders, imprinting disorders, or endocrine disorders of genetic origin. In this review, we discuss the role of mitochondria and the mitochondrial genome as an indicator of sperm quality and fertility.

Linearolactone Induces Necrotic-like Death in Giardia intestinalis Trophozoites: Prediction of a Likely Target.

Linearolactone (LL) is a neo-clerodane type diterpene that has been shown to exert giardicidal effects; however, its mechanism of action is unknown. This work analyzes the cytotoxic effect of LL on Giardia intestinalis trophozoites and identifies proteins that could be targeted by this active natural product. Increasing concentrations of LL and albendazole (ABZ) were used as test and reference drugs, respectively. Cell cycle progression, determination of reactive oxygen species (ROS) and apoptosis/necrosis events were evaluated by flow cytometry (FCM). Ultrastructural alterations were analyzed by transmission electron microscopy (TEM). Ligand–protein docking analyses were carried out using the LL structure raised from a drug library and the crystal structure of an aldose reductase homologue (GdAldRed) from G. intestinalis. LL induced partial arrest at the S phase of trophozoite cell cycle without evidence of ROS production. LL induced pronecrotic death in addition to inducing ultrastructural alterations as changes in vacuole abundances, appearance of perinuclear and periplasmic spaces, and deposition of glycogen granules. On the other hand, the in silico study predicted that GdAldRed is a likely target of LL because it showed a favored change in Gibbs free energy for this complex.

P48 RETROSPECTIVE POSTOPERATIVE NEAR INFRARED SPECTROSCOPY MONITORING ANALYSIS TO DETECT POTENTIAL CRITERIA TO IMPROVE POSTOPERATIVE PREDICTION OF UNFAVOURABLE OUTCOME FOLLOWING AORTIC SURGERY

Abstract Objective Near Infrared Spectroscopy (NIRS) monitoring has become a frequent practice during aortic surgery. The real impact of NIRS in predicting postoperative outcomes, however is still debated, as many cases of “false negative” with severe cerebral damage despite apparently normal NIRS monitoring during surgical procedure. We applied extended retrospective postoperative NIRS monitoring analysis in order to investigate potential criteria to enhance postoperative unfavorable outcome prediction. Materials and Methods Data of NIRS monitoring of 41 patients undergoing aortic surgery (19 acute dissection) were retrospectively analyzed. Partial circulatory arrest with selective bilateral (21 pts) or unilateral (20 pts) cerebral perfusion (CP) was used in all patients. Double channel (R and L) NIRS value was continuously recorded (every 30 sec) from anaesthetic induction to patient’s transfer to ICU. Postoperatively all data were downloaded in excel format and retrospectively analyzed. Baseline, maximum, and minimum value with percentage drop and R/L channel gap were all analyzed considering 5 different phases of surgery: before extracorporeal circulation (EC); in EC before circulatory arrest and selective cerebral perfusion (CA–SCP); in EC following CA–SCP, following EC. Overall time &amp;lt;25% (in each channel) or with a &amp;gt; 20% gap were also evaluated. Results Overall 661±125 values were recorded for each patient. Baseline value on the Left (61±7) was significantly lower then Right (66±12). Maximum drop did not differed in two channels (Fig 1a) but varied according surgical phases (Fig 1). R/L asymmetry also varied according surgical phases with a peak value during rewarming and not during CA–SCP despite unilateral SCP and complexity of procedure (Figure 2 and 3). Conclusion Extended postoperative analysis of NIRS recorded value shows different trend and behavior according surgical phase and cerebral perfusion strategy. Accurate extended NIRS analysis is therefore mandatory in order to improve knowledge of physiological cerebral perfusion during SCP and early identification of patients at high risk of postoperative cerebral complications.

Significance of Seminal Fructose Level in Spermatogenic Activity After Progesterone Treatment

Fructose is the main source of energy for the sperm motility. The degree of fructose utilization is directly proportional to the sperm motility. It could be the cause of negative correlation between sperm motility and semen fructose level. Fructose is a source of energy for the sperm motility. A parallel set of squirrels (Funambulus pennanti) treated with high and low doses of depot medroxy progesterone acetate (Depo provera), a synthetic progesterone for short and long term duration indicated that the spermatogenic activity in the seminiferous tubules was inversely related with the concentrations of seminal fructose. Thus the seminiferous tubules showing total arrest of spermatogenesis and atrophy of Leydig cells- anazoospermic condition, a significant increase in fructose values were observed, slight increase in the fructose values were registered in the oligozoospermic condition whereas a significant decrease in the fructose values were recorded in the partial arrest of spermatogenic activity. The results were supported by the cauda epididymal sperm count, histological changes in the Leydig cells histopathological changes in seminiferous tubules.

Correction of Posttraumatic Medial Growth Arrest of the Distal Tibia in Adolescents.

Partial growth arrest of the medial part of the distal tibial physis following fractures that penetrated the epiphysis is relatively common. We present the results of treatment, based on a protocol of supramalleolar tibial and fibular osteotomy for ankle alignment correction, and contralateral epiphysiodesis of distal tibia and fibula to balance leg length discrepancy (LLD). This case series study describes the results of 7 patients with a median age of 14 years (range = 10-15 years) who were operated in our institution. All were treated by closed or open reduction and internal fixation after Salter-Harris (SH) types 3 and 4 fractures of the distal tibia. All patients had a partial medial growth arrest, distal tibial varus, relative overlengthening of the distal fibula, and slight leg shortening. Contralateral distal tibial and fibular epiphysiodesis to prevent significant LLD, completion of closure of the ipsilateral epiphysis, supramalleolar osteotomy of the distal tibia and fibula, and insertion of a triangular wedge cortical allograft into the tibial osteotomy creating a normal ankle joint orientation. The osteotomy was supported by a medial anatomically contoured locking plate. The fibula was fixed with an intramedullary wire. All patients had uneventful healing of the osteotomy after 6 weeks. At the latest follow-up (mean 3 years, range 1.5-5 years), 6 out of 7 patients reached maturity, and the lateral distal tibial angle was within normal limits. The LLD in all patients was less than 8 mm. Our protocol provides anatomic correction with the restoration of the ankle joint and prevents the progression of LLD. Level IV.